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METHOD OF USING A TRANSGENIC NONHUMAN ANIMAL IN AN IN VIVO TEST METHOD (E.G., DRUG EFFICACY TESTS, ETC.)

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800 - Multicellular living organisms and unmodified parts thereof and related processes

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DocumentTitleDate
20110179502MODULATION OF GM98 (MRF) IN REMYELINATION - The present invention provides compositions and methods for regulating remyelination and promoting oligodendrocyte differentiation by modulating GM98 (also known as MRF) expression and activity. Compositions and methods for treating neuropathies and screening for bioactive agents are also provided herein.07-21-2011
20110179501Methods for Reverting Methylation by Targeting DNMT3A and DNMT3B - Methods for restoring a desired pattern of DNA methylation, inducing re-expression of methylation-silenced tumor suppressor genes (TSGs), and/or inhibiting tumorigenicity both in vitro and in vivo in a subject in need thereof by administering an effective amount of one or more miR-29s sufficient to target one or more of DNMT3A and DNMT3B are disclosed.07-21-2011
20110185439G PROTEIN COUPLED RECEPTORS AND USES THEREOF - The present invention provides GPCR polypeptides and polynucleotides, recombinant materials, and transgenic mice, as well as methods for their production. The polypeptides and polynucleotides are useful, for example, in methods of diagnosis and treatment of diseases and disorders. The invention also provides methods for identifying compounds (e.g., agonists or antagonists) using the GPCR polypeptides and polynucleotides of the invention, and for treating conditions associated with GPCR dysfunction with the GPCR polypeptides, polynucleotides, or identified compounds. The invention also provides diagnostic assays for detecting diseases or disorders associated with inappropriate GPCR activity or levels.07-28-2011
20080276328METHODS FOR IDENTIFYING ANTI-TUMOR AND/OR ANTI-ANGIOGENESIS DRUGS WITH DEOXYNUCLEOSIDE 5'-MONOPHOSPHATE N-GLYCOSIDASE AS THE TARGET - The present invention relates to a novel target for identifying and/or screening antitumor and/or antiangiogenesis agents using the rcl encoded deoxynucleoside 5′monophosphate N-glycosidase.11-06-2008
20130031644AUTONOMOUS LUX REPORTER SYSTEM AND METHODS OF USE - Disclosed are systems for expression of an autonomous lux reporter system in a vertebrate cell, such as mammalian or fish cell. In some examples the lux reporter system is operably connected to a pollutant-inducible DNA response element. Also disclosed are transgenic zebrafish, carrying pollution-inducible response elements, and methods of using such zebrafish to monitor pollutants.01-31-2013
20080276327Methods and Compositions Related to Delivery of Chemical Compounds to Invertebrate Embryos - Disclosed are methods and compositions related to the delivery of chemical compounds to invertebrate embryos.11-06-2008
20100088773MUTATIONS IN LAMA2 GENE OF ZEBRAFISH - The present invention relates to an isolated nucleic acid molecules encoding mutant lama2 gene of zebrafish, mutant zebrafish having mutations in the lama2 gene, fish models containing mutant zebrafish, and uses of the fish models.04-08-2010
20080313748Transgenic Non-Human Animals Comprising the Human Udp-Glucuronosyltransferase 1A (Ugt1a) Gene Locus and Methods of Using Them - The invention provides non-human transgenic animals, and cell lines, host cells, tissues and isolated organs, comprising the human UDP-glucuronosyltransferase IA (UGT1A) gene locus. In one aspect, the endogenous UGT1A gene locus of the non-human transgenic animal has been partially or completely “knocked out.” In another aspect, the invention is directed to drug screening, design and discovery. In another aspect, the invention is directed to determining the toxicity or metabolism of a compound, e.g., a toxin or drug, including environmental, dietary, cosmetic, biological warfare or other known or potentially toxic compounds. In another aspect, the invention is directed to deteuiining the toxicity or metabolism of a compound during a particular metabolic state of an animal, e.g., including pregnancy, stress, diet, age or a particular genotype.12-18-2008
20110191865Novel Gene Disruptions, Compositions and Methods Relating Thereto - The present invention relates to transgenic animals, as well as compositions and methods relating to the characterization of gene function. Specifically, the present invention provides transgenic mice comprising disruptions in PRO227, PRO233, PRO238, PRO1328, PRO4342, PRO7423, PRO10096, PRO21384, PRO353 or PRO1885 genes. Such in vivo studies and characterizations may provide valuable identification and discovery of therapeutics and/or treatments useful in the prevention, amelioration or correction of diseases or dysfunctions associated with gene disruptions such as neurological disorders; cardiovascular, endothelial or angiogenic disorders; eye abnormalities; immunological disorders; oncological disorders; bone metabolic abnormalities or disorders; lipid metabolic disorders; or developmental abnormalities.08-04-2011
20080263685Animal model, cells, and treatment for malignant melanoma - The present invention provides transgenic non-human animal models and cell lines which express a metabotropic glutamate receptor 1 in a melanocyte-specific manner and, as a result, exhibit a predisposition to the development of melanoma. The invention further teaches methods of using the transgenic animals and cell lines to identify therapeutic agents. Diagnostic methods for detecting a melanoma are also provided.10-23-2008
20110203007ASSAYS OF NEURODEGENERATIVE DISORDERS, INCLUDING FRONTOTEMPORAL DEMENTIA AND AMYOTROPHIC LATERAL SCLEROSIS - The invention relates to novel assays for the in vivo analysis of neurodegenerative diseases and the use of such assays to discover therapies capable of modulating such diseases.08-18-2011
20110203008TRANSGENIC MOUSE FOR SCREENING AND FOR STUDIES OF THE PHARMACODYNAMICS AND PHARMACOKINETICS OF LIGANDS ACTING ON THE OESTROGEN RECEPTOR AND ITS INTRACELLULAR RECEPTORS, AND METHOD FOR THE PREPARATION THEREOF - The object of the invention is a method for the production of a non-human transgenic mammal by means of which it is possible to monitor in vivo and in all the tissues the state of activation of any intracellular receptor, utilising a reporter gene inducible by natural or synthetic molecules which modulate the activity of such receptor. The mammal is question is preferably a mouse.08-18-2011
20080256649Novel Acetylcholinesterase Gene Responsible for Insecticide Resistance and Applications Thereof - The invention relates to a novel acetylcholinesterase gene (ace-1) responsible for resistance to organophosphorus and/or carbamates in mosquitoes, which is non-homologous to the 10-16-2008
20100115637MODELS OF THROMBOTIC THROMBOCYTOPENIC PURPURA AND METHODS OF USE THEREOF - The invention relates to the development of an animal model for testing various agents in the treatment of a clotting disorder. More specifically, the invention relates to the use of ultra-large molecular weight multimers of von Willebrand factor (VWF) in various mouse strains to induce thrombotic thrombocytopenic purpura (TTP)-like symptoms for the development of a mouse model of TTP. The invention also provides methods for generating such animal disease models and screening methods for identifying biologically active compounds which are effective in the treatment of TTP.05-06-2010
20130086701CONTROL OF GROWTH AND REPAIR OF GASTRO-INTESTINAL TISSUES BY GASTROKINES AND INHIBITORS - A novel group of gastrokines called Gastric Antrum Mucosal Protein is characterized. A member of the group is designated AMP-18. AMP-18 genomic DNA, cDNA and the AMP-18 protein are sequenced for human, mouse and pig. The AMP-18 protein and active peptides derived from it are cellular growth factors. Surprisingly, peptides capable of inhibiting the effects of the complete protein, are also derived from the AMP-18 protein. Cytoprotection and control of mammalian gastro-intestinal tissue growth and repair (restitution) is facilitated by the use of the proteins, making the proteins candidates for therapies in inflammatory bowel disease and gastric ulcers.04-04-2013
20130036481USE OF PERLECAN DOMAIN V IN TREATING AMYLOIDOGENIC DISEASE - The application reports that perlecan domain V (DV) or the LG3 domain thereof reduces deposition and toxicity of Aβ peptide, the major component of plaques in Alzheimer's disease. Methods of using DV, LG3 and related molecules in treatment of amyloidogenic diseases, particularly Alzheimer's disease, are provided.02-07-2013
20130036482METHOD FOR ASSESSMENT OF POTENTIAL FOR DEVELOPMENT OF DRAVET SYNDROME AND USE THEREOF - Provided is a method of assessing a potential for development of Dravet syndrome with high accuracy, and use thereof. The method according to the present invention of assessing a potential for development of Dravet syndrome includes, with use of a sample taken from a subject, detecting whether or not a mutation is on α-subunit type 1 of voltage-gated sodium ion channel Na02-07-2013
20080307534Methods and Compositions for the Detection and Isolation of Ligands - A method for the detection and isolation of ligands, preferably nuclear receptor ligands, bound to their cognate receptors in live animals, is described. A novel composition comprising 1) a chimeric transcription factor containing a DNA-binding domain, preferably from a non-vertebrate transcription factor, fused to the ligand-binding domain (LBD) of a nuclear receptor, 2) a reporter system, driven by a promoter that contains binding sites for the chosen DNA-binding domain, 3) multiple affinity tags fused to the LBD fusion proteins to facilitate efficient purification, along with specifically associated molecules and 4) sequences required for simultaneous genomic integration of all three components above are described. To make use of the system, expression of the chimeric LBD protein is broadly induced.12-11-2008
20100043082Transgenic Frog Lines and Assays Employing Them - Rhodopsin transgenes driven by rhodopsin promoters were produced, some attached to GFP coding sequences as a fusion construct. When the resulting transgenes were introduced into 02-18-2010
20100333217SCREENING METHOD FOR THE COMPOSITION FOR PREVENTION OR TREATMENT OF OSTEOPOROSIS AND METABOLIC BONE DISEASE USING TALLYHO/JNGJ MOUSE - Provided is a method for screening a composition for preventing or treating an osteoporosis and a metabolic bone disease using a TALLYHO/JngJ mouse, and more particularly, to a method for screening a compound effective in preventing and treating a disease caused by abnormalities of a bone metabolism including an osteoporosis, through assessment of a bone regeneration activity, such as acceleration of osteoblast differentiation, inhibition of osteoclast differentiation, variation of cytokine in a serum, as well as a bone mineral density and a bone mineral content in a femur, using a TALLYHO/JngJ mouse instead of a ovariectomized animal generally used in estimating the efficacy of a new osteoporosis medicine in an animal. The screening method has a simple and stable experiment procedure, and can be used in developing an agent for treating an osteoporosis of men and improving the bone mineral content. Therefore, the method can be used in estimating an indirect efficacy on the metabolic bone disease and the osteoporosis.12-30-2010
20100107263C-REACTIVE PROTEIN (CRP) KNOCKOUT MOUSE - The instant invention relates to a transgenic, non-human animal that carries a mutation in the gene encoding C-reactive protein (CRP). Preferably, the invention relates to an animal comprising a homozygous CRP-deficient mouse and techniques for producing such animals. The invention also relates to organs, tissues, cells, cell lines and sub-cellular fractions derived from such animals. Techniques for generating total or tissue-specific CRP knockout animals are also described. The invention further relates to the use of such knockout animals for the study of the role of CRP proteins in vivo or ex vivo, particularly in relation to its role in inflammatory pathway and in the etiology human diseases.04-29-2010
20090119786Model animal of schizophrenia - A non-human transgenic animal exhibiting schizophrenic symptoms in which a polynucleotide encoding SREB2 whose overexpression in the brain causes schizophrenia and a polynucleotide comprising a promoter are introduced; and a method of screening for a therapeutic agent for schizophrenia, comprising the steps of administrating a test substance to the animal, determining a schizophrenia-related disorder in the animal, and selecting the substance exhibiting a therapeutic effect on schizophrenia are disclosed. According to the present invention, a model animal of schizophrenia in which the genetic background that causes schizophrenia is reflected, and an in vivo screening method for a therapeutic agent for schizophrenia can be provided.05-07-2009
20090007281Animal Model for Assessing Copd-Related Diseases - Methods of diagnosis, markers, and screening techniques and animal models for assessing the severity and/or progression or regression of chronic obstructive pulmonary disease (COPD) and COPD-related diseases are disclosed.01-01-2009
20090019556OASIS GENE-DEFICIENT MOUSE - A mouse that is deficient in the function of the gene for OASIS, and a method for screening for, or evaluating a pharmacological efficacy of, therapeutic agents for osteoporosis using the mouse.01-15-2009
20090307785Transgenic animals for analyzing CYP3A4 cytochrome P450 gene regulation - The invention relates to the generation of non-human transgenic animals comprising a reporter construct for producing a detectable amount of a reporter molecule operably linked to a transcriptional regulatory nucleic acid molecule from the human CYP3A4 gene located between the initiation of transcription site of the gene and a position located 13,000 nucleotides upstream from the site. The invention also relates to the use of these animals for determining the effect of a compound, particularly, but not exclusively, a xenobiotic or steroid, on the regulation of expression of the CYP3A4 gene in a human.12-10-2009
20090307784Methods of Analysing Cell Behaviour - The invention related to a method of imaging a clonal cell line comprising providing a test animal comprising a marker gene, inducing inheritable activation of said marker in at least one cell of said test animal, wherein inheritable activation is induced in fewer than 1 in 27 cells in the tissue of interest, incubating the test animal, and visualising those clonal cells which express the marker gene as a result of the inheritable activation. In particular the invention concerns-methods where the tissue is epidermis, and wherein the visualisation is by confocal microscopy such as wholemount confocal microscopy. The invention also relates to toxicity and carcinogenicity testing using such methods.12-10-2009
20120192294Inhibitors of the Nitration of Amyloid Beta Peptides and Their Uses in the Diagnosis and Treatment of Alzheimer's Disease - The present invention relates to a method for identifying an inhibitor of the aggregation of amyloid-β peptide (Aβ), comprising the steps of a) contacting at least one Aβ-peptide and/or the nitrated forms thereof with at least one candidate inhibitor that potentially specifically binds to a region in said Aβ-peptide capable of being nitrated, and b) detecting said inhibitor specifically binding to said region in said Aβ-peptide through detecting a lack of or a reduced aggregation of said at least one Aβ-peptide. The present invention is further directed at improved methods for treating neuronal degradation and particularly Alzheimer's disease, based on said inhibitor. The present invention is further directed at methods for diagnosing the aggregation of Aβ-peptide in the context of neuronal degradation and particularly Alzheimer's disease.07-26-2012
20130061338SCREENING OF DRUG FOR ATTENTION DEFICIT HYPERACTIVE DISORDER BY USING GIT1 KNOCK-OUT MICE AS A NOVEL ADHD MOUSE MODEL - Provided is a method of using any mammal except humans, in particular, a mammal as an attention deficit hyperactivity disorder model, wherein genes of G protein-coupled receptor kinase interacting protein 1 (GIT1) as a neuronal synapse protein in the brain are knocked out from the mammal. In addition, disclosed is analysis of GIT1 knock-out mice in aspects of molecular biology, cellular biology, electrical biology and animal behavior and, more particularly, a screening method of novel drug, wherein excessive behavior as an attention deficit hyperactive disorder as well as recovery of theta wave in the frontal lobe are observed by administering a candidate material of the drug, thereby inducing recovery of the attention deficit hyperactivity disorder.03-07-2013
20090288177SGRF GENE-MODIFIED MOUSE - A targeting vector was constructed by replacing exon regions in the SGRF gene with appropriate drug marker genes. This vector was transfected into mouse ES cell lines to obtain chimeric mice, which were then crossed with C57BL/6J mice to obtain mice comprising cells in which one SGRF gene alleles was inactivated. By crossing these mice with each other, the present inventors succeeded in producing mice in which both SGRF gene alleles were inactivated. These genetically modified animals can be used to predict the side effects of drugs such as SGRF antagonists.11-19-2009
20090271879ANALOGUES OF (-)-PICROPODOPHYLLIN, SYNTHESIS AND USES THEREOF - Compounds, compositions, methods of making, and methods of using analogues of (−)-picropodophyllin, as well as a transgenic animal model and its use for identifying anticancer agents.10-29-2009
20090055940ZEBRAFISH MODEL OF MLL LEUKEMOGENESIS - The zebrafish mll gene and methods of use thereof are provided.02-26-2009
20090055939Probe for detection and quantification of nitric oxide, and method for detecting and quantifying nitric oxide using the same02-26-2009
20120227118MO-1 CONDITIONAL KNOCK-OUT NON-HUMAN ANIMAL AND USES THEREOF - A conditional knock-out non-human animal is disclosed. Wherein some cells of the non-human animal but not all the cells comprise a disrupted MO-1 nucleic acid sequence, wherein the disruption results in an inability of the non-human animal to produce detectable levels of the MO-1 protein, as assayed by Southern blot analysis.09-06-2012
20120117667NOVEL COELENTERAZINE SUBSTRATES AND METHODS OF USE - An isolated polynucleotide encoding a modified luciferase polypeptide and novel coelenterazine-based substrates. The OgLuc variant polypeptide has at least 60% amino acid sequence identity to SEQ ID NO: 1 and at least one amino acid substitution at a position corresponding to an amino acid in SEQ ID NO: 1. The OgLuc variant polypeptide has at least one of enhanced luminescence, enhanced signal stability, and enhanced protein stability relative to the corresponding polypeptide of the wild-type 05-10-2012
20130067605hnRNP A1 KNOCKOUT ANIMAL MODEL AND USE THEREOF - A nucleic acid construct comprising a genetic engineered heterogeneous nuclear ribonucleoprotein (hnRNP) A1 gene is provided. A transgenic mouse in which the expression of hnRNP A1 gene has been disrupted is also provided. The mouse is useful for studying the role of hnRNP A1 gene in normal and disease states of a neurodegenerative disease or a cancer for developing therapies to treat any of these diseases. Therefore, a method of screening a compound for potential use in prevention and/or treatment of neurodegenerative disease or cancer is further provided.03-14-2013
20130067604Method of Treatment or Prevention of Hair Loss or for the Enhancement of Hair Growth - The present application relates to use of a Midkine family protein for growing hair on a mammal, or in the manufacture of a medicament for growing hair on a mammal, especially for treatment or prevention of different forms of alopecia.03-14-2013
20110023153GENOMIC EDITING OF GENES INVOLVED IN ALZHEIMER'S DISEASE - The present invention provides genetically modified animals and cells comprising edited chromosomal sequences encoding proteins associated with AD. In particular, the animals or cells are generated using a zinc finger nuclease-mediated editing process. Also provided are methods of using the genetically modified animals or cells disclosed herein to study AD development and methods of assessing the effects of agents in genetically modified animals and cells comprising edited chromosomal sequences encoding proteins associated with AD.01-27-2011
20110023152GENOME EDITING OF COGNITION RELATED GENES IN ANIMALS - The present invention provides genetically modified animals and cells comprising edited chromosomal sequences encoding proteins that are associated with cognitive disorders. In particular, the animals or cells are generated using a zinc finger nuclease-mediated editing process. Also provided are methods of assessing the effects of agents in genetically modified animals and cells comprising edited chromosomal sequences associated with cognitive disorders.01-27-2011
20110023148GENOME EDITING OF ADDICTION-RELATED GENES IN ANIMALS - The present invention provides genetically modified animals and cells comprising edited chromosomal sequences encoding proteins associated with addiction disorders. In particular, the animals or cells are generated using a zinc finger nuclease-mediated editing process. The invention also provides zinc finger nucleases that target chromosomal sequence encoding addiction-related proteins and the nucleic acids encoding said zinc finger nucleases. Also provided are methods of using the genetically modified animals or cells disclosed herein to screen agents for addiction and withdrawal side effects and other effects.01-27-2011
20110023147GENOMIC EDITING OF PRION DISORDER-RELATED GENES IN ANIMALS - The present invention provides genetically modified animals and cells comprising edited chromosomal sequences encoding proteins that are associated with cognitive disorders. In particular, the animals or cells are generated using a zinc finger nuclease-mediated editing process. Also provided are methods of using the genetically modified animals or cells disclosed herein to screen agents for toxicity and other effects.01-27-2011
20110023146GENOMIC EDITING OF GENES INVOLVED IN SECRETASE-ASSOCIATED DISORDERS - The present invention provides genetically modified animals and cells comprising edited chromosomal sequences encoding proteins that are associated with a secretase disorder. In particular, the animals or cells are generated using a zinc finger nuclease-mediated editing process. Also provided are methods of using the genetically modified animals or cells disclosed herein to screen agents for toxicity and other effects.01-27-2011
20110023145GENOMIC EDITING OF GENES INVOLVED IN AUTISM SPECTRUM DISORDERS - The present invention provides genetically modified animals and cells comprising edited chromosomal sequences encoding proteins associated with ASD. In particular, the animals or cells are generated using a zinc finger nuclease-mediated editing process. Also provided are methods of using the genetically modified animals or cells disclosed herein to study ASD development and screen agents for assessing their effect on progression or symptoms of an ASD.01-27-2011
20110023144GENOMIC EDITING OF GENES INVOLVED IN AMYOTROPHYIC LATERAL SCLEROSIS DISEASE - The present invention provides genetically modified animals and cells comprising edited chromosomal sequences encoding proteins that are associated ALS. In particular, the animals or cells are generated using a zinc finger nuclease-mediated editing process. Also provided are methods of using the genetically modified animals or cells disclosed herein to screen agents for toxicity and other effects.01-27-2011
20110023143GENOMIC EDITING OF NEURODEVELOPMENTAL GENES IN ANIMALS - The present invention provides genetically modified animals and cells comprising edited chromosomal sequences encoding proteins that are associated with neurodevelopmental disorders. In particular, the animals or cells are generated using a zinc finger nuclease-mediated editing process. Also provided are methods of using the genetically modified animals or cells disclosed herein to screen agents for toxicity and other effects.01-27-2011
20110023141GENOMIC EDITING OF GENES INVOLVED WITH PARKINSON'S DISEASE - The present invention provides genetically modified animals and cells comprising edited chromosomal sequences encoding proteins associated with Parkinson's disease. In particular, the animals or cells are generated using a zinc finger nuclease-mediated editing process. Also provided are methods of using the genetically modified animals or cells disclosed herein to study PD development and screen agents for assessing their effect on progression or symptoms of PD.01-27-2011
20110023140RABBIT GENOME EDITING WITH ZINC FINGER NUCLEASES - The present invention provides a genetically modified rabbit or cell comprising at least one edited chromosomal sequence. In particular, the chromosomal sequence is edited using a zinc finger nuclease-mediated editing process. The disclosure also provides zinc finger nucleases that target specific chromosomal sequences in the rabbit genome.01-27-2011
20110023139GENOMIC EDITING OF GENES INVOLVED IN CARDIOVASCULAR DISEASE - The present invention provides genetically modified animals and cells comprising edited chromosomal involved in cardiovascular disease. In particular, the animals or cells are generated using a zinc finger nuclease-mediated editing process. The invention also provides zinc finger nucleases that target chromosomal sequences involved in cardiovascular disease and the nucleic acids encoding said zinc finger nucleases. Also provided are methods of using the genetically modified animals or cells disclosed herein to screen agents for toxicity and other effects.01-27-2011
20110023138MAMMALIAN ARTIFICIAL CHROMOSOME VECTOR COMPRISING HUMAN CYTOCHROME P450 GENE (CLUSTER) AND NON-HUMAN MAMMALIAN ANIMAL RETAINING THE SAME - This invention relates to a mammalian artificial chromosome vector, which retains a human chromosome 7 fragment comprising human cytochrome P450 genes and is transmittable to progeny, wherein the human chromosome 7 fragment retains a region of approximately 1 Mb±500 Kb in size comprising at least a human CYP3A gene cluster, which region is located between chromosome markers AC004922 and AC073842, and to a non-human mammalian animal retaining the vector.01-27-2011
20110023137FUSION PROTEIN COMPRISING A CASPASE DOMAIN AND A NUCLEAR HORMONE RECEPTOR BINDING DOMAIN AND METHODS AND USES THEREOF - The present invention relates to a fusion protein comprising a Caspase domain or a functionally active variant thereof and a ligand binding domain of a nuclear hormone receptor, a nucleic acid coding for the fusion protein, a vector or cell comprising the nucleic acid, a method of producing the fusion protein, a non-human transgenic animal containing the nucleic acid, the use of the fusion protein for ligand-mediated induction of apoptosis of a cell, or for studying the function of a cell, tissue and/or organ or the use of a transgenic organism for studying the function of a cell at various developmental stages or as a disease model, a method for inducing apoptosis of a cell expressing a fusion protein or for identifying a ligand, or a medicament comprising a fusion protein, the nucleic acid, the vector or the cell, particularly for the treatment of cancer or for or after transplantation, particularly as safety mechanism.01-27-2011
20110023136F1B-TMIR Plasmid Vector and Transgenic Mouse - A trifusion reporter plasmid is described that comprises a plasmid operably coupled to a mammalian FGF1B promoter that is operably coupled to a bioluminescence gene fused to a fluorescence gene fused to a nuclear medical imaging gene. The new reporter allows in vivo or ex vivo detection of gene expression in three different ways, in addition to traditional in vitro detection methods. Transgenic animals containing this new trifusion reporter and uses of same are described.01-27-2011
20110023135USE OF A NEW GENE CODING FOR A NEW MEMBER OF THE MCM2-8 FAMILY IN PHARMACEUTICAL COMPOSITIONS - The use of the human or animal MCM9 gene, or parts of the gene, or transcripts thereof, or antisense nucleic acids able to hybridize with part of the gene or transcripts, or silencing RNA derived from parts of the transcripts and able to repress the MCM9 gene, or proteins or peptidic fragments translated from the transcripts, or antibodies directed against the proteins or peptidic fragments, for the preparation of a pharmaceutical composition for the treatment of a human or animal pathology linked to a dysfunction of the expression of the MCM9 gene, or of human or animal cancers.01-27-2011
20130067603SPERM-SPECIFIC CATION CHANNEL, CATSPER4, AND USES THEREFOR - Nucleic acid and protein sequences relating to a cation channel which is sperm-specific (CatSper4) are disclosed. The CatSper4 protein is shown to be specifically expressed in sperm. Nucleic acids, vectors, transformed cells, transgenic animals, polypeptides, and antibodies relating to the CatSper4 gene and protein are disclosed. Also provided are methods of in vitro fertilization and contraception, methods of identifying modulators of CatSper4 activity, methods of genotyping subjects with respect to CatSper4, and methods of diagnosing and treating CatSper4-mediated disorders, including infertility. Related business methods are also disclosed.03-14-2013
20090007280Ange gene in atopy - The present invention relates to isolated nucleic acid sequences of ANGE, CLLD8 and CLLD7 or sequences complementary or substantially homologous thereto or fragments thereof. Also provided are sequences comprising hybrid nucleic acid sequences from two or more of the genes. Also provided are nucleic acid expression vectors, polypeptides, antibodies to the polypeptides, host cells, non-human transgenic animals and pharmaceutical compositions and agents. Also provided is the use of the nucleic acid sequence and/or protein in medicine and research, methods for diagnosing or determining predisposition to disease or severity of disease, methods for preventing or treating disease, and kits for use in the methods and the use of the nucleic acid sequence and protein in treating or preventing IgE mediated diseases and non-atopic asthma, and in screens for identifying new agents for use in the methods.01-01-2009
20090172828BYDV MP IS A VIRAL DETERMINANT RESPONSIBLE FOR PLANT GROWTH RETARDATION - The present invention concerns the barley yellow dwarf virus (BYDV) and compositions and methods related thereto. In particular in the invention, identifies a movement protein (MP) of BYDV as being responsible for at least one symptom produced as a result of BYDV infection. In certain aspects, the invention concerns a target to inhibit BYDV and to inhibit at least one symptom of BYDV infection, for example, at least plant growth retardation. In particular aspects, the invention relates to screening methods for identifying suppressors of BYDV MP.07-02-2009
20090235367Non-human mammal comprising a modified SERCA2 gene and methods, cells, genes, and vectors thereof - The present invention relates to a non-human mammal in which all cells contain genetic modifications in a Ca09-17-2009
20120233715HUMAN ARTIFICIAL CHROMOSOME VECTOR - A human artificial chromosome vector comprising a human antibody heavy chain gene, a human antibody light chain gene, and a human antibody surrogate light chain gene.09-13-2012
20090013418Trophectodermal Cell-Specific Gene Transfer Methods - The present inventors discovered that genes could be introduced specifically into trophectodermal cells with high efficiency, by infecting blastocysts with viral vectors carrying an arbitrary polynucleotide, or by using a nucleic acid transfection reagent in blastocysts, from which zona pellucida (extracellular matrix covering preimplantation early embryos to protect them from infection of viruses and the like) is removed. This method has no risk of infecting cells of the inner cell mass, which develops into a fetus in the future, with the introduced polynucleotide because the trophectoderm serves as a barrier. The present invention provides methods for introducing foreign genes into only placenta but not fetus, which enables rescue of genetically mutant animals from embryonic lethality due to placental abnormality and allows their birth. Furthermore, it is possible to analyze expression and effect of genes that regulate placental formation or placental function by using these methods.01-08-2009
20090013417Transgenic Animals for Assessing Drug Metabolism and Toxicity in Man - A method of introducing at least one human cytochrome P450 into a non-human animal c ell in which corresponding endogenous P450 enzyme activities have been disabled, thus the method provides a way of using a non-human animal cell to make predictions regarding P450-mediated metabolism in a human. The present invention also provides transgenic non-human animals produced by the method of the invention and uses therefor, especially in assessing xenobiotic/drug metabolism and toxicity.01-08-2009
20090013416PDES AS MODIFIERS OF THE IGFR PATHWAYS AND METHODS OF USE - Human PDE genes are identified as modulators of the IGFR pathway and thus are therapeutic targets for disorders associated with defective IGFR function Methods for identifying modulators of IGFR comprising screening for agents that modulate the activity of PDE are provided01-08-2009
20080320609Diabetes Model Animal - We prepared a transgene comprising human HB-EGF precursor cDNA, as a diphtheria toxin receptor gene, at the downstream of an insulin promoter, and introduced this transgene into a mouse fertilized egg, to produce a transgenic mouse of the present invention. In this mouse, human HB-EGF precursors are expressed specifically in islet beta cells, and by injection of diphtheria toxin, islet beta cells are selectively destroyed, resulting in that the mouse shows diabetes two or three days after the injection. This mouse can be utilized in screening and development of new medicines and therapy protocols for diabetes.12-25-2008
20080295187Accessing the Toxic Potential of Nanomaterials11-27-2008
20080295186Neurotrypsin overexpressing animal11-27-2008
20080295185Transgenic Mouse Models of Hepatitis C Virus (Hcv) and Identification of Hvc Therapeutics11-27-2008
20120102581Multiplexed Luciferase Reporter Assay Systems - Inhibitors of luciferase enzymes are disclosed and find use in multiplexed assays using multiple luciferases and multiple inhibitors, in both in vitro and in vivo embodiments.04-26-2012
20090320147Nonhuman transgenic animal as type 2 diabetes model - The invention provides a non-human transgenic animal as a model of type 2 diabetes manifesting a symptom of type 2 diabetes by excessive expression of the active SREBP-2 protein in pancreatic β-cells by introducing a recombinant DNA in which a DNA encoding the active SREBP-2 protein is disposed under the control of a promoter, and a method for screening therapeutic agents of diabetes using the transgenic animal.12-24-2009
20120124681DNA FRAGMENT AND PHARMACEUTICAL COMPOSITION - Provided are a DNA fragment, a pharmaceutical composition, and the like, which can simplify the period of creating knockout animals. The DNA fragment includes: a detection sequence that codes for a detection marker other than drug resistance (preferably a visually-detectable marker); a resistance sequence that codes for a resistance marker for a drug that inhibits the proliferation of one or more species of at least prokaryotic organisms; a promoter sequence that is located upstream of the resistance sequence and functions in prokaryotic organisms; and a regulatory sequence that is located upstream of all of the above sequences and, only when inserted into a target region of the genome of at least one species of eukaryotic organism, induces the expression of a sequence located downstream. The detection sequence and the resistance sequence are arranged so as to be capable of action.05-17-2012
20100287628Genetically Modified Rat Models for Cancer - This invention relates to the engineering of animal cells, preferably mammalian, more preferably rat, that are deficient due to the disruption of tumor suppressor gene(s) or gene product(s). In another aspect, the invention relates to genetically modified rats, as well as the descendants and ancestors of such animals, which are animal models of human cancer and methods of their use.11-11-2010
20100122355Transgenic Reporter Mouse and Method for Use - A transgenic mammal, including a transgenic mouse, whose genome comprises a transgene, said transgene comprises a neutrophil gelatinase-associated lipocalin (NGAL) promoter gene operably linked to at least one sequence encoding at least one of a fluorescent or bioluminescent protein, wherein the NGAL promoter gene expression in the mouse can be assayed by bioluminescence or fluorescence imaging.05-13-2010
20100122354CDC6S AS MODIFIERS OF THE PTEN/AKT PATHWAY AND METHODS OF USE - Human CDC6 genes are identified as modulators of the PTEN/AKT pathway, and thus are therapeutic targets for disorders associated with defective PTEN/AKT function. Methods for identifying modulators of PTEN/AKT, comprising screening for agents that modulate the activity of CDC6 are provided.05-13-2010
20110289605Animal Model for Osteoarthritis and Intervertebral Disc Disease - Provided herein is a transgenic animal whose genome comprises a first nucleic acid sequence encoding a fusion polypeptide, wherein the fusion polypeptide comprises a Cre recombinase and a mutated ligand binding domain of human estrogen receptor (CreER), wherein the first nucleic acid is operably linked to a chondrocyte-specific promoter and a second nucleic acid sequence encoding a β-catenin polypeptide, wherein the second nucleic acid sequence comprises one or more loxP sequences. Also provided is a method of modifying a transgenic animal comprising administering tamoxifen to the transgenic animal. Also provided are methods of screening for an agent that reduces or prevents Cre-Negative Control one or more symptoms of osteoarthritis or intervertebral disc disease in a subject. Methods for identifying a subject with or at risk of developing osteoarthritis or intervertebral disc disease are also provided, as well as methods of treating or preventing osteoarthritis or intervertebral disc disease in a subject.11-24-2011
20110289604Methods for Identifying Modulating Compounds of Lymphangiogenesis, Means Therefore, Compounds and Uses Thereof - The invention relates to a method for testing whether a compound is capable of inhibiting the development of lymphatic channels or lymphangiogenesis and/or the migration of lymphangioblasts in an non-human animal, a non-human embryo or a cell culture, comprising steps of contacting a compound capable of interacting with a Ccbe1 gene, a transcript thereof or a ccbe1 protein with a non-human animal, a non-human embryo or a cell culture; determining whether said compound inhibits the development of lymphatic channels, lymphangiogenesis and/or migration of lymphangioblasts in said non-human animal, a non-human embryo or a cell culture. The invention further related to a method of determining whether an individual is a carrier of, or is suffering from, or at risk of suffering from, a lymph vessel disorder, and to a medicament comprising Ccbe1, or comprising a nucleic acid encoding Ccbe1, for the treatment of a lymph vessel disorder.11-24-2011
20110296540ASSAY FOR SCREENING ANTIDEPRESSANTS - This invention provides a method for identifying a small molecule as an antidepressant, a method for identifying a small molecule as an anxiolytic, and a method for identifying a small molecule as able to increase dendritic arborization, decrease expression of an immaturity marker, increase expression of a maturity marker, or enhance artificial cerebrospinal fluid-type long-term potentiation in central nervous system. This invention also provides a transgenic mouse model for SSRI-non-responders.12-01-2011
20110296539Mutant Alpha-Synuclein, and Methods Using Same - The present invention relates to a mutant human alpha-synuclein with increased toxicity compared to wild-type alpha-synuclein, or a homologue thereof, wherein the mutant alpha-synuclein or homologue thereof comprises at least one amino acid substitution selected from the group consisting of a substitution at the alanine at position 56 (A56), at the alanine at position 76 (A76), at the methionine at position 127 (M127) and/or at the valine at position 118 (V118), as defined in the claims. Further, the invention relates to a polynucleotide encoding the mutant alpha-synuclein or homologue thereof, or an expression vector comprising said polynucleotide, a cell comprising the polynucleotide or expression vector, as defined in the claims. Also, a non-human animal comprising the cell of the invention is provided, as defined in the claims. Finally, the invention provides methods for identifying a substance that prevents or reduces toxicity of alpha-synuclein, as defined in the claims.12-01-2011
20110296538IN VIVO QUANTITATIVE SCREENING TEST FOR ANTI-METASTASIS TREATMENT EFFICACY - The present invention is directed to methods for evaluating the efficacy of a cancer treatment for (i) inhibiting metastasis in a subject, (ii) inhibiting local cancer cell movement, and (iii) inhibiting cancer cell proliferation. The present invention is further directed to methods for monitoring cell motility in a subject. The present invention is also directed to kits for performing any of the above methods.12-01-2011
20080289054Fish Cancer Model - The present invention is directed to fish whose genome has integrated therein an oncogenic nucleic acid operably linked to a promoter. Methods of making the fish and methods for their use are also provided. The fish may advantageously be utilized in methods of screening for drugs or agents that modulate oncogene-mediated neoplastic or hyperplastic transformation, or that modulate sensitivity to chemotherapy or radiation therapy. Immortal tumor cells lines, methods of making immortal tumor cell lines and methods of their use are also provided. 11-20-2008
20100269180METHODS, COMPOSITIONS AND TRANSGENIC MODELS RELATED TO THE INTERACTION OF T-CADHERIN AND ADIPONECTIN - Disclosed are methods, compositions and transgenic models related to the interaction of T-cadherin and adiponectin.10-21-2010
20100169987ANIMAL MODEL SIMULATING NEUROLOGIC DISEASE - The present invention relates to the development of a pharmacological non-human animal model that associates memory loss to histopathological features found in the brain of a subject having Alzheimer's Disease. In one embodiment, a four-week continuous infusion of a Fe07-01-2010
20110219462G-Protein Coupled Receptor 30 (GPR30) transgenic animals as a model for cardiovascular diseases - The present invention relates to use of the GPR30 gene for diagnosis and treatment of cardiovascular disorders, especially cardiomyopathy. The present invention also relates to a GPR30 deficient animal model, more specifically to a mouse in which the GPR30 gene is disrupted and which exhibits a cardiomyopathy, a tissue and a cell of the mouse and a process of producing the same. The present invention further relates to use of said knockout mouse as a model of cardiovascular diseases, especially cardiomyopathy, and a method of screening a compound useful for the prevention and/or treatment of cardiovascular diseases, especially cardiomyopathy, using the knockout mouse.09-08-2011
20110219463METHODS OF SCREENING AGENTS FOR ACTIVITY USING TELEOSTS - The present invention provides methods of screening an agent for activity using teleosts. Methods of screening an agent for angiogenesis activity, toxic activity and an effect cell death activity in teleosts are provided. Methods of screening an agent for an activity in the brain or central nervous system in zebrafish are provided. The invention further provides high throughput methods of screening agents in multi-well plates.09-08-2011
20090276863Protein formulations comprising s1-5 - The present inventors discovered that knockout mice whose S1-5 gene function is lost develop age-related diseases or symptoms. Histological analysis in such knockout mice revealed that bone mineral content, bone mineral density, and bone strength were decreased, and the number of osteoclasts in bone tissues was increased. Analysis of osteoclast-forming ability using bone marrow cells derived from the knockout mice revealed that osteoclast-forming ability is enhanced and osteoclasts are larger in the knockout mice than in wildtype mice. When purified S1-5 protein was added to this in vitro system, osteoclast-forming ability was inhibited.11-05-2009
20090183267MOUSE MODELS CARRYING A KNOCK-OUT MUTATION OF THE QPCT-GENE - The present invention provides a knock-out non-human animal, in particular a mouse carrying a Qpct knock-out mutation. The present invention additionally provides the respective cells and cell lines and methods and compositions for evaluating agents that affect Qpct, for use in compositions for the treatment of Qpct-related diseases.07-16-2009
20100115635Methods for Assessing the Delivery of Exogenous Agents - This invention provides methods, compositions and kits for rapid determination of the delivery of exogenous agents both in vitro and in vivo, including without limitation siRNA, microRNA, a ribozyme or an antisense molecule, any of which may target, bind to, or inactivate the mRNA of the gene of interest expressed in the cells. The methods, compositions and kits utilize a promoter-reporter construct whereby successful non-viral nucleic acid delivery leads to an up-regulation of reporter signals thus providing a quantitative, sensitive and rapid means of detection, validation and monitoring.05-06-2010
20090151012Animal Model Having a Chimeric Human Liver and Susceptible to Human Hepatitis C Virus Infection - The present invention features a non-human animal model that is susceptible to infection by human hepatotrophic pathogens, particularly human hepatitis C virus (HCV). The model is based on a non-human, immunocompromised transgenic animal having a human-mouse chimeric liver, where the transgene provides for expression of a urokinase-type plasminogen activator in the liver. The invention also features methods for identifying candidate therapeutic agents, e.g., agents having antiviral activity against HCV infection. The animals of the invention are also useful in assessing toxicity of various agents, as well as the activity of agents in decreasing blood lipids.06-11-2009
20120110682Animal Model for Toxicology and Dose Prediction - The invention relates to the use of fetal tissues to generate a tissue model in a non-human animal. The tissue model comprises target tissues allowed to progress through development in vivo in a non-human host in order to obtain tissues having a mature phenotype that can be used to assess toxicity and/or efficacy of an agent.05-03-2012
20090151011Chimeric Non-Human Animal and Use Thereof - This invention provides: a pluripotent cell derived from a non-human animal comprising foreign DNA that encodes a desired protein in such a manner that the expression of the desired protein is regulated by the control region of a gene expressed in certain cells and/or tissue, wherein the foreign DNA is bound to a nucleic acid fragment comprising a promoter/the whole or part of 5′ non-translational region/a leader sequence coding region derived from a gene expressed in certain cells and/or tissue, and wherein in said cell one or more drug resistant marker genes used for introducing the foreign DNA into the genome have been removed; a chimeric non-human animal that is prepared from the pluripotent cell and highly expresses the desired protein, or a progeny thereof; a method for producing a desired protein using the chimeric animal; and a method for analyzing in vivo function of a desired gene using the chimeric animal.06-11-2009
20100122356PIG MODEL FOR PSORIASIS - The present invention relates to a genetically modified pig as a model for studying psoriasis. The modified pig model displays one or more phenotypes associated with psoriasis. Disclosed is also a modified pig comprising a mutation in the endogenous ILK-I Ra, JunB/cJun, CD18, IKK2, and/or LIG1 gene, and/or a human, porcine and/or murine PPARs, PPAR-δ, lκB-α, STAT3c, Integrin beta 1, Integrin alpha 2, MEK1, Amphiregulin, BMP-6, VEGF, JunBΔec-JunΔep, IL-I a, TGF.beta 1, CD18 hypo, Cre/lkk2FL/FL, Dsg1, SCCE, TGF-a, TNF-a, IL-20, IFN-g, LIG1 KO, KGF, IL-6, PAFR1 Cre/lkk2FL/FL, IL1 R, Dsg3, IFN-gamma, p40, ILI Ra, IKK2, JunB/c-Jun, and/or LIG1 gene, transcriptional and/or translational product or part thereof. The invention further relates to methods for producing the modified pig; and methods for evaluating the effect of a therapeutical treatment of psoriasis, for screening the efficacy of a pharmaceutical composition, and a method for treatment of human being suffering from psoriasis are disclosed.05-13-2010
20130219528NOVEL TREATMENT OF PROSTATE CARCINOMA - Disclosed herein are naphthoquinone analogs, such as plumbagin, pharmaceutical compositions that include naphthoquinone analogs, such as plumbagin, and methods of treating diseases and/or conditions such as cancer with naphthoquinone analogs, such as plumbagin. Also included are combination therapies wherein a naphthoquinone analog, such as plumbagin, and a hormone therapy agent are provided to a subject suffering from a condition such as cancer.08-22-2013
20100100974Models of Malignant Brain Cancer, and Therapeutic siRNAs Against Oncogenic Signaling Pathways, and Methods and Kits for Uses Therefor - Methods for screening compounds to treat an oncological disorder regulated through a tumor-inducing pathway are provided. The compounds are administered to non-human animal subjects having a disease model, so that the subjects display pathology symptoms that correspond to the oncological disorder in humans. The subjects carry a regulatable transgene expression, of which is associated with tumor formation, and further carry regulatable genes for suppression of tumor formation. The disease-pathology symptoms are induced using a site-specific recombination system to induce expression of the transgene associated with tumor formation and negatively regulate or eliminate the genes for suppression of the tumor formation. The methods further involve analyzing tumor formation in subjects administered the compound and comparing appearance and amount of tumors in the subjects administered the compound with control subjects not administered the compound. Also included are a vector for engineering a disease model and a kit for its use.04-22-2010
20110197288Transgenic animal for screening of compounds that modulate cell proliferation, and its use in the pharmaceutical field - The present invention relates to a transgenic non-human mammalian animal whose genome incorporates a biosensor of the activity of modulators of cell proliferation consisting of a DNA sequence that comprises the luciferase reporter transgene ligated downstream of a promoter sequence of the CYCB2 gene, this sequence promoter/reporter being flanked by HS4 insulator sequences at each of its 3′ and 5′ sides.08-11-2011
20090249498Methods of diagnosing alzheimer's disease and markers identified by set association - The present disclosure relates to genetic markers and methods of diagnosing and screening for late-onset Alzheimer's disease (LOAD). As such, the disclosure encompasses a whole-genome association analysis of single nucleotide polymorphisms (SNPs) of which a number are located within the GRB2-associated binding protein 2 (GAB2) gene as well as other markers associated with other genes. The disclosure identifies two novel haplotypes within the GAB2 gene, i.e., a LOAD risk-enhancing and a LOAD risk-decreasing haplotype. These haplotypes modify LOAD risk differentially in combination with APOE alleles. Further encompassed are therapeutic methods and agents of decreasing the deterioration of cells associated with LOAD.10-01-2009
20090255001Parkinson's Disease-Related Gene GRK5 and Uses Thereof - Large-scale SNP analyses conducted on subjects in a Parkinson's disease patient group and a normal control group led to the successful identification of a gene (GRK5) associated with Parkinson's disease. In addition, it was newly discovered that phosphorylation of α-synuclein is promoted by enhanced expression of the GRK5 gene, and as a result, the formation of soluble α-synuclein oligomers is promoted, leading to Parkinson's disease. The present invention enables the assessment of Parkinson's disease as well as the screening of therapeutic agents for Parkinson's disease using as an index the expression of GRK5 gene.10-08-2009
20090249499SPERM-SPECIFIC CATION CHANNEL, CATSPER4, AND USES THEREFOR - Nucleic acid and protein sequences relating to a cation channel which is sperm-specific (CatSper4) are disclosed. The CatSper4 protein is shown to be specifically expressed in sperm. Nucleic acids, vectors, transformed cells, transgenic animals, polypeptides, and antibodies relating to the CatSper4 gene and protein are disclosed. Also provided are methods of in vitro fertilization and contraception, methods of identifying modulators of CatSper4 activity, methods of genotyping subjects with respect to CatSper4, and methods of diagnosing and treating CatSper4-mediated disorders, including infertility. Related business methods are also disclosed.10-01-2009
20090249500SYSTEM FOR MONITORING BACTERIAL TUMOR TREATMENT - A method to follow the progress of tumor treatment in subjects utilizes bacteria that have been modified to express a fluorescent protein. The method can also monitor expression of genes associated with the bacteria that produce therapeutic agents during the course of treatment, optionally against a background of fluorescence generated by the tumor itself. The method permits visualization of the progress of treatment in live subjects so that treatments can be modified according to their efficacy.10-01-2009
20090222931NOVEL IDENTIFIED ONCOGENE WITH KINASE-DOMAIN (NOK) - A newly identified oncogene with kinase-domain (NOK) and its encoded polypeptide, and vectors, fusions, host cells and transgenic animals comprising the said nucleotide sequence. Furthermore, the present invention also describes the methods for diagnosing diseases including tumor and the methods for screening agents capable of inhibiting the occurrence and/or metastasis of tumor.09-03-2009
20090187998Method of screening for agents to treat heart failure - The invention provides a method of identifying candidate agents to test for treating heart failure involving diastolic impairment, the method comprising: testing an agent to determine whether it (a) binds to serum response factor (SRF), (b) reduces SRF binding to a serum response element (SRE), or (c) reduces SRF protein levels in a cell; wherein if the agent does one or more of (a), (b), and (c), it is identified as a candidate agent.07-23-2009
20090187997Cre-lox based gene knockdown constructs and methods of use thereof - The present invention relates to vectors, compositions and methods for conditional, Cre-lox regulated, RNA interference. The vectors allow for spatial and temporal control of miRNA expression in vivo.07-23-2009
20090089888Sour/Acid Taste Receptors Assays, Genes and Proteins - Taste receptor PC-1-L3/PC-2-L1 is provided. Methods and systems for screening for tastants and receptor modulators are provided. Knock out and transgenic animals, methods of detecting polymorphisms, and methods of correcting taste defects are also provided.04-02-2009
20120144505TARGETED AND REGIONAL CELLULAR ABLATION IN ZEBRAFISH - A system including: (i) a methodology for targeted cellular ablation in zebrafish; (ii) a methodology for regional cellular ablation in zebrafish. These methodologies are used to identify genetic components that regulate cellular regeneration and to identify drug compounds that influence cellular regeneration for the purpose of developing therapies for degenerative conditions. Transgenic zebrafish disclosed herein contain transgenic constructs composed of: (i) cell and/or tissue-type specific regulatory elements (e.g. promoter and/or enhancer regions) which delimit expression of operably linked gene product(s) to discrete cellular populations; (ii) a gene product that promotes cellular ablation composed of a pro-drug conversion system capable of converting nontoxic pro-drugs into cytotoxic drugs, which is expressed alone or in connection with; (iii) a reporter gene product that allows selective detection of cells expressing the reporter—both prior to (initial cells) and following cellular ablation (regenerated cells). Here we describe genetic delivery of a pro-drug converting system in order to enable targeted cellular ablation in zebrafish, Transgenic zebrafish of this invention provide a high-throughput system for genetic dissection of the process of cellular regeneration and, compound screening for the discovery of drugs capable of promoting cellular regeneration.06-07-2012
20100100973CRANIAL AND VERTEBRAL DEFECTS ASSOCIATED WITH LOSS-OF-FUNCTION OF NELL1 - The mouse Nell1 cDNA and amino acid sequences are disclosed. Also disclosed is a Nell1 knock-out mouse with several bone- and cartilage-related defects. On the molecular level, the loss of Nell1 function led to reduced expression of certain extracellular matrix proteins. The disclosure here provides new tools for studying bone and cartilage development as well as new drug screening and treatment strategies for bone- and cartilage-related diseases and conditions.04-22-2010
20110173708NOVEL GENE DISRUPTIONS, COMPOSITIONS AND METHODS RELATING THERETO - The present invention relates to transgenic animals, as well as compositions and methods relating to the characterization of gene function. Specifically, the present invention provides transgenic mice comprising disruptions in PRO226, PRO257, PRO268, PRO290, PRO36006, PRO363, PRO365, PRO382, PRO444, PRO705, PRO1071, PRO1125, PRO1134, PRO1155, PRO1281, PRO1343, PRO1379, PRO1380, PRO1387, PRO1419, PRO1433, PRO1474, PRO1550, PRO1571, PRO1572, PRO1759, PRO1904, PRO35193, PRO4341, PRO4348, PRO4369, PRO4381, PRO4407, PRO4425, PRO4985, PRO4989, PRO5737, PRO5800, PRO5993, PRO6017, PRO7174, PRO9744, PRO9821, PRO9852, PRO9873, PRO10196, PRO34778, PRO20233, PRO21956, PRO57290, PRO38465, PRO38683 or PRO85161 genes. Such in vivo studies and characterizations may provide valuable identification and discovery of therapeutics and/or treatments useful in the prevention, amelioration or correction of diseases or dysfunctions associated with gene disruptions such as neurological disorders; cardiovascular, endothelial or angiogenic disorders; eye abnormalities; immunological disorders; oncological disorders; bone metabolic abnormalities or disorders; lipid metabolic disorders; or developmental abnormalities.07-14-2011
20110173707System for the Determination of Molecules Altering the Function of Interferon, Method Therefor and Compounds Altering Interferon Activity - In a first aspect, cyclic peptides are provided identified as molecules altering the interferon activity, namely, inhibiting interferon response. Moreover, the present invention relates to a transgenic animal or parts thereof and a method for the determination of molecules and compounds altering the function of interferons, in particular, type I and type II interferon. In particular, said transgenic animal or parts thereof contain large parts of exogenous chromosomal DNA, namely interferon responsive DNA promoter elements operably linked with a nucleic acid sequence encoding a reporter or marker molecule. These a transgenic animal or parts thereof are useful in the methods according to the present invention.07-14-2011
20110173706NOVEL GPR101 TRANSGENIC MICE AND METHODS OF USE THEREOF - The invention provides transgenic animals comprising a disruption in the endogenous GPR101 gene and methods of producing such transgenic animals. The invention further provides methods of identifying compounds that modulate GPR101 receptor proteins.07-14-2011
20090288176Novel Gene Disruptions, Compositions and Methods Relating Thereto - The present invention relates to transgenic animals, as well as compositions and methods relating to the characterization of gene function. Specifically, the present invention provides transgenic mice comprising disruptions in PRO286, PRO706, PRO1800, PRO4354, PRO6029, PRO9739, PRO20044, PRO28631 or PRO34128 genes. Such in vivo studies and characterizations may provide valuable identification and discovery of therapeutics and/or treatments useful in the prevention, amelioration or correction of diseases or dysfunctions associated with gene disruptions such as neurological disorders; cardiovascular, endothelial or angiogenic disorders; eye abnormalities; immunological disorders; oncological disorders; bone metabolic abnormalities or disorders; lipid metabolic disorders; or developmental abnormalities.11-19-2009
20090158447TLR ligand and IL-1 Response-Injured Animal Model - The present invention provides a TLR ligand/IL-1 response-impaired non-human animal model wherein IL-6 production responding to a TLR ligand/IL-1 is impaired, a method for screening a substance promoting or suppressing a response to a TLR ligand/IL-1 by using the TLR ligand/IL-1 response-impaired non-human animal model, and a method for screening a prophylactic/therapeutic agent for atopic dermatitis-like inflammatory skin disease. A non-human animal model unresponsive to a TLR ligand/IL-1 is generated wherein whole or a part of an endogenous gene of the non-human animal encoding IκB-ζ is inactivated by a gene mutation such as destruction, deletion, or substitution, a function of expressing IκB-ζ is deleted, and a IL-6 production responding to a TLR ligand and IL-1 is impaired. Moreover, the promoter or suppressor for a TLR ligand/IL-1 response and the prophylactic/therapeutic agent for atopic dermatitis-like inflammatory skin disease are screened by using the non-human animal and a test substance.06-18-2009
20080216180Animal model for cancer, methods of producing the same and associated methods of use - A transgenic animal having a somatic cell in which at least one allele of an endogenous p53 and Pten gene is functionally disrupted is provided. The cell of the animal may be heterozygous or, more preferably, homozygous for the gene disruptions. The animals of the invention can be used to evaluate the efficacy of novel therapeutics and to identify novel points of therapeutic intervention for cancer. In certain embodiments, the transgenic animal is a transgenic mouse having functionally disrupted endogenous p53 and Pten genes. This mouse can be used to identify agents that inhibit the development of cancers, namely bladder cancers in humans in vivo. Nucleic acid constructs for functionally disrupting an endogenous p53 and Pten gene in a host cell, recombinant vectors including the nucleic acid construct, and host cells into which the nucleic acid construct has been introduced are also encompassed by the invention09-04-2008
20100275275HADHs as Modifiers of the p21 Pathway and Methods of Use - Human HADH genes are identified as modulators of the p21 pathway, and thus are therapeutic targets for disorders associated with defective p21 function. Methods for identifying modulators of p21, comprising screening for agents that modulate the activity of HADH are provided.10-28-2010
20100287627Transgenic Zebrafish Models for Neurodegenerative Diseases - The present invention relates to zebrafish models for neurodegenerative disorders that allow screening of compounds for their ability to protect and/or regenerate neurons in vivo in a whole vertebrate organism. The present invention also provides methods of identifying gene targets for neuroprotective compounds, compounds that regenerate neurons and compounds that promote neurogenesis.11-11-2010
20100287626METHOD OF SCREENING PTP ZETA ACTIVITY PROMOTER OR INHIBITOR - An object of the present invention is to provide a remedy for dysfunction of central monoamine pathway, a method for screening a PTPζ inhibitor or activator, which is useful as a remedy for gastric ulcer caused by 11-11-2010
20100287625VEGF VARIANTS - This invention relates to a Vascular Endothelial Growth Factor (VEGF) polypeptide, which polypeptide lacks an amino acid sequence encoded by exon 5 of the VEGF gene. This variant of VEGF is capable of eliciting activities associated with VEGF whilst showing resistance to proteolytic degradation. The invention provides uses of this protein and nucleic acid sequences from the encoding genes in the diagnosis, prevention and treatment of disease.11-11-2010
20100138942USE OF THE AUGMENTER OF LIVER REGENERATION PROTEIN AS AN APOPTOSIS REGULATOR - The invention relates to a new use of the protein called Augmenter of Liver Regeneration (Alrp) in the regulation and control of apoptosis in mammals.06-03-2010
20100138937Method for diagnosis of severity and prediction of recurrence in eosinophilic inflammatory disease - A method for diagnosis of the severity of a condition in an eosinophilic inflammatory disease such as nasal polyp or for prediction of the recurrence of the disease, the method comprising detecting H-PGDS induced by eosinophilic leukocytes accumulated in a lesion or determining pGD06-03-2010
20110209227METHODS FOR THE DIAGNOSIS AND TREATMENT OF BONE DISORDERS - This invention pertains to chemometric methods for the analysis of chemical, biochemical, and biological data, for example, spectral data, for example, nuclear magnetic resonance (NMR) spectra, and their applications, including, e.g., classification, diagnosis, prognosis, etc., especially in the context of bone disorders, e.g., conditions associated with low bone mineral density, e.g., osteoporosis.08-25-2011
20100138941METHOD FOR SCREENING IMMUNE MODULATOR - Disclosed is a method for screening an immune modulator. More specifically, disclosed is a method of screening an immune modulator, an anticancer agent and an agent for treating autoimmune diseases, which regulate the cell surface expression level of gp96, using the binding of the region of amino acids 54-192 of AIMP1 to the region of amino acids 699-799 of AIMP1, set forth in SEQ ID NO: 18. Also disclosed is a method of diagnosing autoimmune diseases using the binding.06-03-2010
20120144507F1B-TMIR PLASMID VECTOR AND TRANSGENIC MOUSE - A trifusion reporter plasmid is described that comprises a plasmid operably coupled to a mammalian FGF1B promoter that is operably coupled to a bioluminescence gene fused to a fluorescence gene fused to a nuclear medical imaging gene. The new reporter allows in vivo or ex vivo detection of gene expression in three different ways, in addition to traditional in vitro detection methods. Transgenic animals containing this new trifusion reporter and uses of same are described.06-07-2012
20090265795Methods of Inhibiting Multiple Cytochrome P450 Genes with siRNA - The present invention relates to siRNAs that are targeted to RNAs encoding two or more enzymes of a subfamily of cytochrome P450 (CYP) enzymes, along with vectors, cells, and kits comprising the siRNAs. The invention further relates to methods of decreasing expression of two or more CYP subfamily genes in a non-human animal, animals in which expression of two or more CYP subfamily genes has been decreased, and methods of using such animals to study the function of cytochrome P450 enzymes.10-22-2009
20100146642Methods and compositions relating to PBK1 - The invention relates to compositions comprising, and methods utilizing PBK1 protein and DNA, including a method of detecting type 1 diabetes; a mammalian pancreas-derived cell comprising a recombinant nucleic acid encoding a PBK1 protein; a method of identifying a PBK1 modulator; a pharmaceutical composition for treatment of type 2 diabetes in a subject; a method of screening for an agent that treats a metabolic disease; delivery of PBK-1 DNA to a subject to stimulate pancreatic beta cell differentiation and/or regeneration; a method for stimulating cell differentiation and/or regeneration in a pancreatic beta cell; usage of transgenic mice with targeted deletion or overexpression of the PBK-1 gene to test efficacy and specificity of PBK-1 modulator compounds.06-10-2010
20080289053Methods and systems for identifying modulators of longevity - Methods of treating disorders such as neurofibromatosis-1 are provided, including methods in which catalytic antioxidants such as metalloporphyrins are administered. Methods of regulating longevity, and methods and systems for screening for modulators of aging or longevity, are also provided. In addition, related transgenic animals are described.11-20-2008
20080295188DRUG AND METHOD FOR PROLIFERATING NATURAL KILLER CELLS11-27-2008
20090158448DNA ENCODING POLYPEPTIDE CAPABLE OF MODULATING MUSCLE-SPECIFIC TYROSINE KINASE ACTIVITY - Disclosed are DNA encoding a polypeptide which can modulate the activity of a muscle-specific tyrosine kinase, and others. The DNA is selected from the following members (a) to (d): (a) DNA comprising a specific nucleotide sequence; (b) DNA comprising a nucleotide sequence capable of hybridizing with a specific nucleotide sequence under stringent conditions; (c) DNA comprising a nucleotide sequence encoding an amino acid sequence having the substitution, deletion and/or addition of one or several amino acid residues in a specific amino acid sequence; and (d) DNA comprising a nucleotide sequence having 90% or higher homology to a specific nucleotide sequence.06-18-2009
20090328241MITOCHONDRIAL-NUCLEAR EXCHANGED CELLS, TISSUES, ORGANS AND ANIMALS - Provided herein are mitochondrial-nuclear exchanged cells and animals comprising mitochondrial DNA (mtDNA) from one subject and nuclear DNA (nDNA) from a different subject. Methods for producing a mitochondrial-nuclear exchanged animal and animals made by the methods are provided. Also provided are methods of screening for agents useful for treating a disease or disorder using mitochondrial-nuclear exchanged animals or cells, tissues or organs thereof.12-31-2009
20090328240Genetically modified mice as predictors of immune response - The invention is directed to novel genetically modified organisms and uses thereof. In particular, the invention is directed to novel genetically modified mice and uses of such mice to assess the immunogenic potential of human therapeutic antigens and to predict immune responses.12-31-2009
20090328239BLOOD VESSEL IMAGING AND USES THEREFOR - Methods are disclosed for analyzing representations of one or more structures in the body of a subject (e.g., a human subject or other animal subject) to glean information about the health of the subject or to evaluate the subject's response to a therapy or other condition. Aspects of the invention relate to obtaining structural information from casts (e.g., vascular casts from animal models) and using the information as a reference for evaluating structures in the body of a subject. Methods are disclosed for diagnosing, staging, grading, and monitoring diseases. Methods also are disclosed for targeting treatments, monitoring the effectiveness of therapies, and/or screening or validating therapies based analyzing structures (e.g., vascular structures) in a subject and comparing them to reference structures observed in casts obtained from models (e.g., animal models) of related diseases or conditions.12-31-2009
20080289052Method of Constructing Animal Having Cancer Cells Transplanted Thereinto - A cell culture support is first prepared that is coated on a surface with a polymer the hydration force of which changes in a temperature range of 0-80° C.; cancer cells are then cultivated on the support in a temperature region where the polymer has weak hydration force; thereafter, the culture solution is adjusted to a temperature at which the polymer has a stronger hydration force, whereby the cultured cancer cells are detached; the detached cancer cells are then transplanted to a specified site of an animal on which transplantation is to be performed; this method is an efficient way of cancer cells transplantation.11-20-2008
20090313710Nonalcoholic Steatohepatitis Model Animal and Fatty Liver Model Animal - Disclosed is a nonhuman animal showing the symptoms of human nonalcoholic steatohepatitis which is obtained by transplanting human hepatocytes into an immunodeficient hepatopathic nonhuman animal to produce a chimeric nonhuman animal and then transplanting human hepatocytes that are propagated in the body of the chimeric nonhuman animal into an immunodeficient hepatopathic nonhuman animal of the same species as the immunodeficient hepatopathic nonhuman animal described above, as well as a nonhuman animal showing the symptoms of human fatty liver which is obtained by transplanting human hepatocytes into an immunodeficient hepatopathic nonhuman animal to produce a chimeric nonhuman animal.12-17-2009
20080201787Transgenic mouse whose genome comprises a homozygous disruption of its alpha1G gene, a method of preparing the same and use thereof - The disclosure concerns a method for resistance of epilepsy by suppressing the function of alpha 1G protein of T-type calcium channels, use of suppressor of alpha 1G protein for prevention or treatment for epilepsy, knockout mice resisting epilepsy by disrupting alpha 1G subunit of T-type calcium channel, and preparation method thereof. The α1G-knockout transgenic mouse can be used for investigating the relationship between diseases particularly neuropathy or psychopathy and the function of α1G T-type calcium channel via various behavioral tests since α1G subunit is mainly expression in central nervous system (CNS) and pheripheral nervous system (PNS). Further, the α1G-knockout transgenic mouse can be used for screening antileptic agents.08-21-2008
20100146646METHOD OF MONITORING RETINOPATHY - There is presently provided methods of monitoring retinopathy in a live transgenic, non-human animal, the methods comprising providing a live transgenic non-human animal having a retinal pathology or a pre-disposition for a retinal pathology, wherein a nucleic acid molecule encoding a fluorescent protein under control of a GFAP promoter is integrated into the genome of the transgenic non-human animal; and detecting in vivo in the retinal glia of the transgenic non-human animal fluorescence levels of the fluorescent protein.06-10-2010
20100138939PIG MODEL FOR ATHEROSCLEROSIS - The present invention relates to a genetically modified pig as a model for studying atherosclerosis. The modified pig model displays one or more phenotypes associated with atherosclerosis. Disclosed is also a modified pig comprising a mutation in the endogenous ApoE gene or part thereof and/or LDL gene or part thereof, and/or LDL receptor gene, and/or transcriptional and/or translational product or part thereof. The invention further relates to methods for producing the modified pig; and methods for evaluating the effect of a therapeutical treatment of atherosclerosis; methods for screening the efficacy of a pharmaceutical composition; and a method for treatment of a human being suffering from atherosclerosis are disclosed.06-03-2010
20100138936Transgenic Mice and Use Thereof as an Experimental Model - The invention relates to the use of an expression vector construction coding for the functional HLA-DPal03β401 complex specifically identified by anti-HLA-DP antibodies, in order to create transgenic mice. The invention also relates to the use of the transgenic mice obtained, such as for the comparative preclinical study of the efficacy of vaccine candidates in order to asses the risks associated with the unwanted induction of an autoimmune disease and in order to determine a therapeutic strategy.06-03-2010
20130219529PROBE FOR A HAIR CELL, AND LABELLING METHOD FOR A HAIR CELL USING THE PROBE FOR A HAIR CELL - Provided are a novel probe for a hair cell for clearly identifying various conditions of a hair cell, and a labelling method for a hair cell using the probe for a hair cell, more particularly, a probe for a hair cell containing, as an active agent, at least one kind selected from staining compounds represented by one of the general formulae (I) and (II), and a labelling method for a hair cell using the probe for a hair cell.08-22-2013
20090031434ANIMAL MODELS FOR OBESITY AND NEURODEGENERATIVE DISEASES - A transgenic non-human animal is disclosed, the animal having a nucleic acid inserted in its genome, wherein the presence of the inserted nucleic acid in the genome of the animal results in expression of an agent, which agent is encoded by a nucleotide sequence in the genome of the animal, and wherein the agent inhibits the ability of a leptin to activate an Ob-Rb receptor. Uses of the animal and methods of identifying compounds using the animal are also disclosed.01-29-2009
20120198574Targeted cell death - The present invention provides compositions and methods for studying neuropathy. The compositions and methods provided herein are particularly useful for screening agents of therapeutic and/or diagnostic potential.08-02-2012
20130219527Conditional Mst Overexpressing Construct And Conditional Myostatin Overexpressing Transgenic Mouse - Provided herein are novel nucleic acid sequences, vectors comprising such nucleic acid sequences, host cells comprising such vectors, and transgenic animals comprising such nucleic acid sequences, and related molecules and methods relating thereto. Such novel nucleic acid sequences, vectors comprising such nucleic acid sequences, host cells comprising such vectors, and transgenic animals comprising such nucleic acid sequences, and related molecules and methods provide conditional overexpression of genes, such as myostatin, and transgenic animals conditionally overexpression genes, such as myostatin.08-22-2013
20090178145Methods and targets for identifying compounds for regulating angiogenesis - The present invention provides methods for identifying genes and proteins that may regulate angiogenesis. The genes identified may be used as markers for the disease onset and progression and to measure efficacy of a therapeutic. The present invention also provides methods to screen agents that are capable of regulating angiogenesis. The present invention also provides methods of identifying therapeutic compounds that may treat various disorders by regulating the expression and activity of genes and proteins identified.07-09-2009
20080244762T1R HETERO-OLIGOMERIC TASTE RECEPTORS AND CELL LINES THAT EXPRESS SAID RECEPTORS AND USE THEREOF FOR IDENTIFICATION OF TASTE COMPOUNDS - The present invention relates to the discovery that the T1R receptors assemble to form functional taste receptors. Particularly, it has been discovered that co-expression of T1R1 and T1R3 results in a taste receptor that responds to umami taste stimuli, including monosodium glutamate. Also, it has been discovered that co-expression of the T1R2 and T1R3 receptors results in a taste receptor that responds to sweet taste stimuli including naturally occurring and artificial sweeteners.10-02-2008
20090165151CANINE TRANSIENT RECEPTOR POTENTIAL V2 (CTRPV2) AND METHODS OF SCREENING FOR TRPV2 CHANNEL MODULATORS - A recombinant canine TRPV2 channel which has been prepared by cDNA cloning and polymerase chain reaction techniques is disclosed. Expression systems for these channels and an assay using the expression systems are also disclosed. The recombinant TRPV2 channel can be used in assays to evaluate compounds which directly or indirectly interact with or bind to TRPV2 channel.06-25-2009
20100154068FLUORESCENT MOUSE MODEL - The present invention relates to compositions and methods useful for detecting and/or measuring, e.g., intracellular signaling in vivo. More particularly, compositions and methods are provided, which include transgenic animals, that are useful in mapping and examining, e.g., calcium fluctuations in vivo between and within populations of cells in real time. Methods for screening for candidate compounds that effect, e.g., intracellular calcium signaling are also provided.06-17-2010
20090165152Mesothelin Vaccines and Model Systems - Mesothelin can be used as an immunotherapeutic target. It induces a cytolytic T cell response. Portions of mesothelin which induce such responses are identified. Vaccines can be either polynucleotide- or polypeptide-based. Carriers for raising a cytolytic T cell response include bacteria and viruses. A mouse model for testing vaccines and other anti-tumor therapeutics and prophylactics comprises a strongly mesothelin-expressing, transformed peritoneal cell line.06-25-2009
20090038020HUMAN ALBUMIN ANIMAL MODELS FOR DRUG EVALUATION, TOXICOLOGY AND IMMUNOGENICITY STUDIES - An animal model is provided which is genetically engineered to express human serum albumin, and such animals may be advantageously used in assessing drugs, vaccines or other therapeutic compounds that may be used in humans. In addition, an animal model is provided which does not manufacture its own albumin and which has been injected with human serum albumin. Through the use of these animal models, drugs and other chemicals can be more accurately assessed in physiological environments that reflect the conditions to be expected in humans, and such models will be useful in assessing new drugs and evaluating toxic substances for potential dangers as carcinogens, mutagens, etc. Other applications include evaluating immunological properties of various albumin-engineered proteins which might be administered to humans as therapeutics or vaccines, and research of disease states, such as genetic diseases, to provide further insight in treating these diseases.02-05-2009
20120036588METHOD FOR OBSERVING GAD67-POSITIVE CELL IN TRANSGENIC ANIMAL - A method for observing glutamate decarboxylase 67-positive cells in a transgenic mouse includes providing the transgenic mouse in which a nucleic acid sequence encoding green fluorescent protein is inserted in a frame within exon 1 of an endogenous glutamate decarboxylase 67 gene, whereby the transgenic mouse is capable of a functional expression of the green fluorescent protein in place of the endogenous glutamate decarboxylase 67 gene. Then, the glutamate decarboxylase 67-positive cells which are specifically visualized by the expression of the green fluorescent protein can be observed. The method may further include analyzing a function or morphology of the GABAergic neurons based on the observation of the glutamate decarboxylase 67-positive cells where the glutamate decarboxylase 67-positive cells are specifically visualized corresponding to a cell distribution of GABAergic neurons.02-09-2012
20090019554TARGETED CELL DEATH - The present invention provides compositions and methods for studying neuropathy. The compositions and methods provided herein are particularly useful for screening agents of therapeutic and/or diagnostic potential.01-15-2009
20090025095Method for Evaluating Compound Using Barlp and Substance for Regulating Eating and Body Weight - It is intended to provide a method for evaluating a compound which regulates eating or body weight characterized by comprising the steps of introducing a BARLP gene and preparing a cell expressing BARLP; bringing a test compound into contact with the cell; and detecting a specific binding of the test compound to the BARLP and a method for evaluating a compound further comprising the step of evaluating a test compound using a nonhuman genetically-engineered animal in which the BARLP gene is inactivated. According to this invention, knowledge about a relationship between BARLP and biological functions is obtained and a method for evaluating a compound targeting BARLP and a BARLP ligand obtained by the evaluation can be provided.01-22-2009
20090083867Use of Antagonists of Cxcl13 or Cxcr5 for Treating Wounds of Fibrotic Diseases - The invention provides the use of an antagonist of CXCL 13 or CXCR5 activity in the preparation of a medicament for the prevention and/or inhibition of pathological scarring; as well as the use of such antagonists in the preparation of a medicament for the prevention and/or inhibition of fibrotic disorders; and the use of such antagonists in the preparation of a medicament for the prevention and/or treatment of a chronic wound. Medicaments or methods of the invention are particularly suitable for use in keloids or venous ulcers. Suitable antagonists of CXCL13 or CXCR5 activity may be any compound capable of inhibiting the CXCL13/CXCR5 signalling pathway. The invention also provides a model of aberrant wound healing, which may lead to pathological scar formation, or to chronic wound formation.03-26-2009
20120079611TL1A MODEL OF INFLAMMATION FIBROSIS AND AUTOIMMUNITY - This invention relates transgenic animals that overexpress TL1A in a tissue specific manner to model inflammatory bowel disease (IBM such as colitis, Crohn's disease and ulcerative colitis, fibrosis, and related inflammatory diseases and conditions. TL1A transgenic animals constitutively express both TL1A and GFP in lymphoid and myeloid cell lineages, allowing convenient identification and sorting of immune cells involved in IBD disease progression, such as T-cells, antigen presenting cells (APC), and dendritic cells (DC). TL1A transgenic animals may be induced to exhibit gross fibrosis, or isolated cells may be implanted into immunodeficient mice to establish colitis.03-29-2012
20090064350DETECTION AND TREATMENT OF DRUG ASSOCIATED ANGIOEDEMA - The present invention relates to an in vitro method of diagnosing a drug-associated angioedema or a predisposition thereto in a subject being suspected to having developed or of having a predisposition to develop a drug-associated angioedema or in a subject being intended to be treated with a drug associated with the development of angioedema, the method comprising determining in a biological sample from said subject the presence or absence of a disease-associated mutation in a nucleic acid molecule regulating the expression of or encoding coagulation factor XII; wherein the presence of such a mutation is indicative of a drug-associated angioedema or a predisposition thereto.03-05-2009
20090064349Chimeric Avian-Based Screening System Containing Mammalian Grafts - The present invention relates to animal model systems comprising a chimera between an avian embryo and a mammalian organism. Specifically, chimeric model systems comprising normal, diseased or genetically transformed mammalian cells and tissues transplanted into avian embryos, and uses thereof for in vivo testing of drugs and therapeutic modalities are disclosed.03-05-2009
20090083868Increasing lifespan by modulation of WWP-1 and UBC-18 - Ubiquitin ligase wwp-1 and ubiquitin conjugating enzyme ubc-18 are identified in nematodes as mediators of dietary restriction induced longevity and therefore as targets for modulation of lifespan in animals. Methods of screening for compounds that modulate longevity by assaying wwp-1 ubiquitination pathway parameters are provided, as are related systems. In addition, methods of using wwp-1 and/or ubc-18 to modulate longevity or delay onset of age-related diseases are described.03-26-2009
20090083866TRANSGENIC ROSA26-LUCIFERASE MICE FOR BIOLUMINESCENT IMAGING - The invention relates to non-human transgenic animals expressing bioluminescent markers03-26-2009
20080263684Pik4ca As Modifier of the Rac Pathway and Methods of Use - Human PIK4CA genes are identified as modulators of the RAC pathway, and thus are therapeutic targets for disorders associated with defective RAC function. Methods for identifying modulators of RAC, comprising screening for agents that modulate the activity of PIK4CA are provided.10-23-2008
20080263683Megsin/Rage/Inos-Overexpressing Renal Disease Model Animals and Methods for Evaluating Compounds Using the Model Animals - Triple Tg (megsin/RAGE/iNOS-Tg) was created by crossing megsin-Tg with RAGE/iNOS-Tg. The megsin/RAGE/iNOS-Tg develops marked pathologies of diabetic nephropathy unfound in conventional models at early stages, and various pathological conditions such as glomerular hypertrophy were observed uniformly in the megsin/RAGE/iNOS-Tg mice. In addition, it was also found that animals exhibiting these symptoms were useful as a disease model animal for diabetic nephropathy. Specifically, the disease model animals of the present invention overexpress the megsin gene, a gene encoding the receptor for advanced glycation end-products, and an inducible nitric oxide synthase gene. As a result, accompanying kidney function disorders of glomerular failure develop at early stages.10-23-2008
20090222934Pre-B Cell Proliferation and Lymphoblastic Leukemia/High-Grade Lymphoma in MIR155 Transgenic Mice - A transgenic non-human animal, such as a mouse, has a genome that include a nucleic acid construct having at least one transcriptional regulatory sequence capable of directing expression in B cells of the animal, wherein the transcriptional regulatory sequence is operably linked to a nucleic acid encoding a miR155 gene product. A method of testing the therapeutic efficacy of an agent in treating or preventing a lymphoproliferative condition includes assessing the effect(s) of the agent on a transgenic non-human animal.09-03-2009
20080282362Non-invasive real-time in vivo bioluminescence imaging of local Ca+ dynamics in living organisms - A method for bioluminescence imaging in an animal is provided. The method comprises providing a whole animal containing a transcriptionally active nucleic acid sequence encoding a Ca11-13-2008
20090205056METHOD OF SCREENING FOR MODULATORS OF MAP3K11 IN LIVER CANCER CELLS - Detection of expression of the provided protein kinase in cancers is useful as a diagnostic, for determining the effectiveness of drugs, and determining patient prognosis. The encoded polypeptides further provides a target for screening pharmaceutical agents effective in inhibiting the growth or metastasis of tumor cells.08-13-2009
20110145936Genetically Modified Rat Models for Pharmacokinetics - The present invention provides a desired rat or a rat cell which contains a predefined, specific and desired alteration rendering the rat or rat cell predisposed to drug transport sensitivity or resistance drug transport resistance or sensitivity. Specifically, the invention pertains to a genetically altered rat, or a rat cell in culture, that is defective in at least one of two alleles of a drug transporter gene such as the Slc7a11 (NC_005101.2) gene, the Abcb1 (NC_005103.2) gene, etc. The present invention also provides a desired rat or a rat cell which contains a predefined, specific and desired alteration rendering the rat or rat cell predisposed to drug transport sensitivity or resistance drug transport resistance or sensitivity. Specifically, the invention pertains to a genetically altered rat, or a rat cell in culture, that is defective in at least one of two alleles of a drug transporter gene.06-16-2011
20090222933Human Liver Cancer Cell Line - The present invention relates to a human hepatoma-derived cell line, LH86, liver cell cultures, non-human animal models, artificial livers, liver assist devices, screening assays, and other applications of the cell line as an investigational tool.09-03-2009
20090260091Methods and animal model for analyzing age-related macular degeneration - Methods for testing candidate drugs for treatment of age-related macular degeneration are provided. Ccl2-deficient, and Ccr2-deficient mice are used to determine the effect of candidate drugs and treatments on development of age-related macular degeneration. Also provided is a Ccl2-deficient, Ccr2-deficient dual knockout mouse, which is a useful animal model for age-related macular degeneration.10-15-2009
20100175140Leucine-rich repeat kinase (LRRK2) drosophila model for parkinson's disease: wildtype1 (WT1) and G2019S mutant flies - Mutations in the leucine-rich repeat kinase (LRRK2) gene cause late-onset autosomal dominant Parkinson's disease (PD) with pleiomorphic pathology. Previously, we and others found that expression of mutant LRRK2 causes neuronal degeneration in cell culture. Here we used the GAL4/UAS system to generate transgenic 07-08-2010
20100169985Transgenic Mouse Models for Diseases Caused by mtDNA Mutations and Related Methods - Animal models and methods wherein homoplasmic and heteroplasmic mtDNA mutation(s) are induced in an animal (e.g., a mouse) to cause or facilitate the development of a disorder (e.g., disease, malformation, defect, abnormality or other disorder). In at least some embodiments, the mtDNA mutation(s) will cause or facilitate the development of an age-related disorder, such as a cardiac disease, cardiomyopathy, muscle disease, cancer, abnormaly in tissues of high cellular turnover, heart dysfunction, graying of hair, alopecia, auditory function loss, cochlear degeneration, immune cell loss, anemia, male germ cell loss leading to lack of sperm and infertility, skeletal muscle mass loss (sarcopenia), neurodegeneration, increased presence of apoptotic markers, and loss of bone mass.07-01-2010
20100169986Conditional Mst Overexpressing Construct and Conditional Myostatin Overexpressing Transgenic Mouse - Provided herein are novel nucleic acid sequences, vectors comprising such nucleic acid sequences, host cells comprising such vectors, and transgenic animals comprising such nucleic acid sequences, and related molecules and methods relating thereto. Such novel nucleic acid sequences, vectors comprising such nucleic acid sequences, host cells comprising such vectors, and transgenic animals comprising such nucleic acid sequences, and related molecules and methods provide conditional overexpression of genes, such as myostatin, and transgenic animals conditionally overexpression genes, such as myostatin.07-01-2010
20120246745Methods for Screening for Agents that Affect Development - The present invention provides an animal toxicity model that can be used to screen agents that may cause or increase the occurrence of a developmental defect. The invention also provides methods and compositions for creating such an animal toxicity model, as well as methods and kits for using these animal models.09-27-2012
20100162415TRANSGENIC MICE EXPRESSING HUMANIZED VEGF - The present invention generally relates to humanized VEGF and non-human transgenic animals expressing it. The transgenic animals are also useful to study VEGF-related therapies.06-24-2010
20100186098TRANSGENIC ANIMAL MODELS OF PARKINSON'S DISEASE - The present invention provides transgenic animal models of Parkinson's disease. More specifically, the present invention provides a transgenic rodent animal containing a nucleic acid molecule which encodes a mutant human LRRK2 protein. The transgenic animal of the present invention recapitulates cardinal Parkinson's disease symptoms and characteristics. The present invention also provides methods of screening for a therapeutic agent useful for treating Parkinson's disease by utilizing such transgenic rodent animal.07-22-2010
20100186097CELL-BASED RNA INTERFERENCE AND RELATED METHODS AND COMPOSITIONS - The invention provides, among other things, methods for performing RNA interference in stem cells and methods for using the stem cells in vivo.07-22-2010
20120198573Agents that Reduce Neuronal Overexcitation - The present invention provides methods of identifying candidate agents for treating excitotoxicity-related disorders. The present invention further provides methods for treating excitotoxicity-related disorders.08-02-2012
20100263064ANIMAL MODEL FOR CHRONIC OBSTRUCTIVE PULMONARY DISEASE AND CYSTIC FIBROSIS - A nonhuman transgenic mammal is described whose genome comprises a promoter construct operably linked to a heterologous DNA encoding an epithelial sodium channel β subunit, wherein said promoter construct directs expression of the epithelial sodium channel β subunit in lung epithelial cells of said animal, and wherein said transgenic mammal has increased lung mucus retention as compared to the corresponding wild-type mammal. The animal is useful in screening compounds for activity in treating lung diseases such as cystic fibrosis and chronic obstructive pulmonary disease.10-14-2010
20100263063MOUSE MODELS WITH ENHANCED ESSENTIAL TREMOR AND PREPARATION METHOD THEREOF - Disclosed herein are an α1/CaV3.1 double knockout mouse or α10-14-2010
20100263062METHODS FOR SCREENING AND COMPOUNDS THAT PROTECT AGAINST AMYLOID DISEASES - The disclosure provides methods and compositions useful for screening inhibitors of aggregation mediated proteotoxicity. The disclosure provides transgenic animals and cell useful for such screening. Also provided are compounds useful for inhibiting aggregation mediated proteotoxicity in a subject.10-14-2010
20100263061Properdin Modulation of Alternative Pathway and Uses Thereof - This invention relates to selective activation of the alternative pathway (AP) using anti-Properdin antibodies. Specifically, the invention relates to methods for treating an AP complement-mediated pathology or AP mediated condition in a subject by contacting the subject with an anti-Properdin antibodies. Likewise, properdin knockout transgenic non-human mammals and their use are provided.10-14-2010
20100192235HUMAN CHRONIC LYMPHOCYTIC LEUKEMIA MODELED IN MOUSE BY TARGETED TCL1 EXPRESSION - Transgenic animals containing a nucleic acid sequence encoding TCL1 operably linked to transcriptional control sequences directing expression to B cells are described. Such transgenic animals provide a useful animal model system for human B cell chronic lymphocytic leukemia.07-29-2010
20080209580Mouse developing visceral fat type obesity and diabetes - An object of the present invention is to provide a mouse which has the characteristics of early developing visceral fat type obesity and also has concurrent diabetes and hyperlipemia and in which the trait is genetically established and recessively inherited. An ICR-derived mouse strain, Daruma, spontaneously developing obesity, exhibiting autosomal recessive inheritance for the trait of spontaneously developing obesity, and becoming obese only in the homozygous type is provided.08-28-2008
20100162416Multi-stage stem cell carcinogenesis - The present invention relates to a system of multi-stage stem cell carcinogenesis and a method of generating such multi-stage stem cell carcinogenesis system. Various stages of cancer stem cells can be generated from normal stem cells via mutagenesis. The system of the present invention enables monitoring changes in the ability of cells to transition from one stage of carcinogenesis to another and to identify genetic pathways and molecules that influence carcinogenesis. The present invention also enables a high-throughput and nonbiased screening for targets that preferentially affect cancer stem cells relative to non-cancer stem cells or their derivatives during stem cell carcinogenesis, thus is useful in developing anti-cancer therapeutics.06-24-2010
20100242123MODELS OF ATHEROSCLEROSIS, HYPERLIPIDEMIA, LIPOPROTEIN OXIDATION AND BLOOD VESSEL INFLAMMATION AND METHODS FOR MAKING AND USING THEM - The invention provides genetically altered fish of the family Cyprinidae, or genus 09-23-2010
20100242124COMPOSITIONS AND METHODS FOR THE TREATMENT AND PREVENTION OF ULCERATIVE COLITIS AND COLON CANCER AND SCREENING METHODS TO IDENTIFY SAME - The instant invention is based, at least in part, on the discovery that T-bet maintains host commensal relationships in the gastrointestinal tract. Accordingly, this invention provides methods of treating and/or preventing ulcerative colitis, and/or colon cancer, and/or preventing colonization of a subject's gastrointestinal tract with commensal bacteria that promote ulcerative colitis as well as methods of identifying agents that treat and prevent the same.09-23-2010
20100251393TRANSGENIC ANIMALS - A transgenic animal such as a transgenic snake or other reptile that expresses a heterologous expression product is described, along with methods of making the same. In general, the animal comprises cells containing a sequence encoding the heterologous expression product. The sequence encoding the heterologous expression product is integrated into the genome of the animal (e.g., in some or all cells thereof, and in some embodiments into germ cells thereof). The sequence encoding the heterologous expression product is, in general, operatively associated with an expression sequence or promoter. The animals are useful for, among other things, testing of repellents, testing of toxicological compounds, as teaching aids, for venom production, etc.09-30-2010
20100146644TRANSGENIC NON-HUMAN ANIMAL - A transgenic non-human animal genetically modified to have a dysfunctional 26S-proteasome in some or all cells, which may exhibit phenotypic and/or neuropathological symptoms similar to those exhibited by individuals with a neurogenerative disorder.06-10-2010
20100235926Hairless Transgenic Animal - The present invention provides a hairless transgenic nonhuman animal used in the development of a therapy for dermatitis such as human atopic dermatitis and drug discovery. Specifically, the present invention provides a transgenic nonhuman animal, into which recombinant DNA comprising a heparin-binding EGF gene and a type 2 keratin gene promoter for regulating expression of the above gene has been introduced.09-16-2010
20110131667Tumor Model System Useful to Study Multistage Cancer - The present invention relates to a method of developing a Tumor Model System. The invention deals with a tumor model system with adhesion deprived cells. This observation provides a new method for primary detection of transformation of adhesion-deprived cells and tumorigenicity. The adhesion-deprived cells are capable of metastasizing at distant sites and the model system includes both the tumor formation and metastasis.06-02-2011
20110004947COMPOSITIONS AND METHODS FOR OSTEOGENIC GENE THERAPY - The present disclosure provides compositions and methods for increasing bone growth and/or enhancing wound healing, for example, fracture repair. The disclosure provides recombinant nucleic acids useful for promoting bone growth. For example, the disclosure provides recombinant nucleic acids that encode a fibroblast growth factor-2 (FGF-2) analog. The disclosure also provides vectors and cells incorporating these nucleic acids, as well as FGF-2 analogs encode by them. The disclosure also provides a mouse system of bone marrow transplantation and methods for producing as well as methods for using the system. Methods for inducing division and/or inducing differentiation of a hematopoietic stem cell are also provided, as are methods for enhancing bone growth and/or wound repair (for example, fracture repair).01-06-2011
20100235928TRANSGENIC ANIMALS FOR ASSESSING DRUG METABOLISM AND TOXICITY - The present invention relates to transgenic non-human animals, tissues or cells derived therefrom and methods of producing them. The transgenic non-human animals or tissues or cells derived therefrom provide a system capable of expressing human proteins responsible for drug metabolism in place of the homologous endogenous non-human animal proteins and for the controlled expression of human genes introduced into the animal so that the expression of the human genes is regulated in a manner more closely analogous to that seen in vivo in humans.09-16-2010
20100212029NOVEL ASSAYS UTILIZING NICOTINIC ACETYLCHOLINE RECEPTOR SUBUNITS - The present invention is in the field of identification and characterization of novel insecticidal target sites and, in particular, relates to host cells, assays and antibodies thereto.08-19-2010
20100251392METHODS FOR ASSESSING THE DELIVERY OF EXOGENOUS AGENTS - This invention provides methods, compositions and kits for rapid determination of the delivery of exogenous agents both in vitro and in vivo, including without limitation siRNA, microRNA, a ribozyme or an antisence molecule, any of which may target, bind to, or inactivate the mRNA of the gene of interest expressed in the cells. The methods, compositions and kits utilize a promoter-reporter construct whereby successful non-viral nucleic acid delivery leads to an up-regulation of reporter signals thus providing a quantitative, sensitive and rapid means of detection, validation and monitoring.09-30-2010
20100138938METHOD OF PRODUCING A MULTICHIMERIC MOUSE AND APPLICATIONS TO STUDY THE IMMUNOPATHOGENESIS OF HUMAN TISSUE-SPECIFIC PATHOLOGIES - The invention relates to a method of producing a multichimeric mouse comprising a functional xenogenic (human) immune system restricted to the MHC class I and/or class II molecules (HLA molecules) of the xenogenic species solely, and a functional tissue. The invention relates also th the use of the multichimeric mouse obtainable by said method, to study the immunopathogenesis of tissue-specific diseases (infectious, tumoral or auto-immune pathologies) and to their applications to design and test vaccines or immunotherapeutic agents against these pathologies.06-03-2010
20090249501CISD2-Knockout Mice and Uses Thereof - The present invention is related to a Cisd2 knockout mouse with phenotype comprising mitochondrial breakdown and dysfunction, wherein Cisd2 is defined as SEQ ID NO. 1. The present invention is also related to a mouse model of Wolfram Syndrome 2 (WFS2) disease consisting of a Cisd2 knockout mouse. The present invention is further related to a method for screening a candidate agent for preventing or treating WFS2 disease.10-01-2009
20110023151GENOME EDITING OF ABC TRANSPORTERS - The present invention provides genetically modified animals and cells comprising edited chromosomal sequences encoding ABC transporter proteins. In particular, the animals or cells are generated using a zinc finger nuclease-mediated editing process. Also provided are methods of assessing the effects of agents in genetically modified animals and cells comprising edited chromosomal sequences encoding ABC transporter proteins.01-27-2011
20110023150GENOME EDITING OF GENES ASSOCIATED WITH SCHIZOPHRENIA IN ANIMALS - The present invention provides genetically modified animals and cells comprising edited chromosomal sequences associated with schizophrenia. In particular, the animals or cells are generated using a zinc finger nuclease-mediated editing process. The invention also provides zinc finger nucleases that target chromosomal sequence associated with schizophrenia and the nucleic acids encoding said zinc finger nucleases. Also provided are methods of assessing the effects of agents in genetically modified animals and cells comprising edited chromosomal sequences associated with schizophrenia.01-27-2011
20110023142Genetically Modified Rat Models for Cytokine-Cytokine Signaling Pathways - The present invention relates to the engineering of animal cells, preferably mammalian, more preferably rat, that are deficient due to the disruption of gene(s) or gene product(s) resulting in cytokine-cytokine mediated autoimmune and inflammatory disease. In another aspect, the invention relates to genetically modified rats, as well as the descendants and ancestors of such animals, which are animal models of human autoimmune and inflammatory disease and methods of their use. Specifically, the invention pertains to a genetically altered rat, or a rat cell in culture, that is defective in at least one of two alleles of a cytokine gene such as the Faslg gene, the Fas gene, etc. In one embodiment, the cytokine gene is the Faslg gene. In another embodiment, the cytokine gene is one of several known cytokine genes, such as Fas, IFNγ, TNF-α, IL-2, IL-10, and IL-12. The inactivation of at least one of these cytokine alleles results in an animal with a higher susceptibility to cytokine-cytokine mediated autoimmune and inflammatory disease induction. In one embodiment, the genetically altered animal is a rat of this type and is able to serve as a useful model for cytokine-cytokine mediated autoimmune and inflammatory disease and as a test animal for autoimmune and other studies.01-27-2011
20100122357HUMAN ALBUMIN ANIMAL MODELS FOR DRUG EVALUATION, TOXICOLOGY AND IMMUNOGENICITY STUDIES - An animal model is provided which is genetically engineered to express human serum albumin, and such animals may be advantageously used in assessing drugs, vaccines or other therapeutic compounds that may be used in humans. In addition, an animal model is provided which does not manufacture its own albumin and which has been injected with human serum albumin. Through the use of these animal models, drugs and other chemicals can be more accurately assessed in physiological environments that reflect the conditions to be expected in humans, and such models will be useful in assessing new drugs and evaluating toxic substances for potential dangers as carcinogens, mutagens, etc. Other applications include evaluating immunological properties of various albumin-engineered proteins which might be administered to humans as therapeutics or vaccines, and research of disease states, such as genetic diseases, to provide further insight in treating these diseases.05-13-2010
20100138940TRANSGENIC PIG AS A MODEL OF ALZHEIMER'S DISEASE - The present invention relates to a modified pig as a model for studying Alzheimer's disease. The modified pig model displays one or more phenotypes associated with Alzheimer's disease. Disclosed is also a modified pig comprising a modified human and/or porcine APP gene, and/or PS1 gene, and/or a transcriptional and/or translational product or part thereof. The invention further relates to methods for producing the modified pig; and methods for evaluating the effect of a therapeutical treatment of Alzheimer's disease; methods for screening the efficacy of a pharmaceutical composition; and a method for treatment of a human being suffering from Alzheimer's disease are disclosed.06-03-2010
20100138935Detection of cellular stress - We provide reporter gene constructs incorporating nucleic acid sequences from a promoter region of a gene or set of genes whose expression is modified in response to external or internal changes in the cellular environment such as biochemical stress or toxic conditions. The promoters are operatively linked to nucleic acid sequences chosen on the basis of the ease with which their transcription and/or translation products may be assayed so that the reporter gene constructs can provide a system capable of detecting intracellular conditions. Also described are transfected cell lines including the constructs and transgenic non-human animal models including the constructs.06-03-2010
20100095387METHODS AND REAGENTS FOR SCREENING NEW DRUGS AND FOR TREATING ION PUMP ASSOCIATED DISORDERS AND DISEASES - The invention relates to fragments of a mammalian nervous system protein, agrin, and to their use as a screening and therapeutic agents in controlling neural activity associated with the function of the Na04-15-2010
20100071079METHODS FOR TREATING AUTOIMMUNE AND CHRONIC INFLAMMATORY CONDITIONS USING ANTAGONISTS OF CD30 OR CD30L - The invention provides methods of treating autoimmune and chronic inflammatory conditions by administering agents that hinder the CD30/CD30L interaction, combination treatments, and methods of treating conditions resistant to treatment with TNFα inhibitors by administering agents that inhibit signal transduction by CD30 or IL-1. Included also are treatments involving concurrently administering agents that block the CD30/CD30L interaction and agents that antagonize the IL-4/IL-4R interaction. Additionally provided is an animal model for screening candidate agents for their efficacy in treating conditions that are resistant to treatment with TNFα inhibitors.03-18-2010
20100199360ENHANCER-CONTAINING GENE TRAP VECTORS FOR RANDOM AND TARGETED GENE TRAPPING - The present invention relates to a novel class of gene trap vector (enhanced gene trap vectors, eGTV) for efficiently identifying silent or weakly expressed target genes in mammalian genomes, methods of their production and methods for identifying and mutating target genes by using the enhanced gene trap vectors. The gene trap vectors of the present invention can also be used for inducing the expression of silent genes and enhancing the expression of weakly expressed genes. The use of the enhanced gene trap vectors for creating transgenic organisms to identify gene function and to validate pharmaceutical compounds prior to clinical applications is a further aspect of the present invention.08-05-2010
20110113494Serine Hydroxymethyltransferase as Target for Herbicides - The present invention relates to serine hydroxymethyltransferase (E.C. 2.1.2.1) as novel target for herbicides, and to nucleic acid sequences encoding a polypeptide with the biological activity of a serine hydroxymethyltransferase, which, when not present, bring about growth retardation symptoms and chlorotic leaves, comprising the nucleic acid sequence SEQ ID No:3, and functional equivalents of the abovementioned nucleic acid sequence or the nucleic acid sequence SEQ ID NO:7 and functional equivalents of the abovementioned nucleic acid sequence. Moreover, the present invention relates to the use of the abovementioned nucleic acid sequences, of functional analogs of the SEQ ID NO:3 or SEQ ID NO:7 or of polypeptides encoded by one of the abovementioned nucleic acid sequences in a method for identifying herbicidally active compounds which inhibit serine hydroxymethyltransferases, and to the use of these compounds which have been identified by the method as herbicides.05-12-2011
20100169988MEANS AND METHODS FOR ISOLATING AND DETERMINING NOVEL TARGETS FOR THE TREATMENT OF NEURODEGENERATIVE, NEUROLOGICAL OR NEUROPSYCHIATRIC DISORDERS AND COMPOSITIONS COMPRISING THE SAME - A novel method of identifying and obtaining molecules interacting with neurodegenerative, neurological or neuropsychiatric disorder-associated proteins is provided, which is suitable for drug screening and drug development. Furthermore, drugs and drug targets for the therapeutic intervention of neurodegenerative, neurological or neuropsychiatric disorders, in particular Alzheimer's disease are described.07-01-2010
20110067121Transgenic mice having a human major histocompatibility complex (MHC) phenotype, experimental uses and applications - The present invention-relates to transgenic mice and isolated transgenic mouse cells, the mice and mouse cells comprising a disrupted H2 class I gene, a disrupted H2 class II gene, a functional HLA class I transgene, and a functional HLA class II transgene. In embodiments, the transgenic mouse or mouse cells are deficient for both H2 class I and class II molecules, wherein the transgenic mouse comprises a functional HLA class I transgene and a functional HLA class II transgene. In embodiments, the transgenic mouse or mouse cell has the genotype HLA-A203-17-2011
20110067120Iduronidase knock-out mouse - The present invention relates to a α-L-iduronidase knock-out mouse. More particularly, this invention relates to a α-L-iduronidase knock-out mouse to be designed for developing a treatment or an agent for mucopolysaccharidosis type I (Hurler syndrome or Hurler-Scheie syndrome) as an animal model.03-17-2011
20090276864TRANSGENIC ANIMALS WITH REDUCED MAJOR URINARY PROTEIN PRODUCTION - The present invention relates to a transgenic animal having substantially reduced major urinary protein (uMUP) production. The present invention also relates to methods of producing such animals, and to the uses of such animals.11-05-2009
20090222932ALZHEIMER'S DISEASE ANIMAL MODEL, METHOD FOR OBTAINING SAME AND USES THEREOF - The invention relates to a transgenic non-human animal which can be used as a non-human animal model for studying Alzheimer's disease (AD) and which is characterized in that: it contains a heterologous polynucleotide (transgene) which is inserted in the genome thereof and which comprises the nucleotide sequence of the complete human APP gene together with the regulatory sequences thereof; and it has an endogenous expression pattern similar to that of the hAPP gene in humans. The inventive model can be used to study AD and in the screening of potentially-useful compounds for the prevention and/or treatment of AD.09-03-2009
20090165150DIRECTED COMPLEMENTATION WITH REMOVABLE GENE OF INTEREST - The invention provides an improved directed complementation method for generating a conditionally tumorigenic mouse cell. In a directed complementation method, the tumorigenicity of a conditionally tumorigenic mouse cell depends on either the expression of an inducible recombinant oncogene or the expression of a recombinant gene of interest that functionally complements an uninduced recombinant oncogene. The invention provides a method of producing a tumorigenic mouse cell containing an uninduced oncogene, a recombinant gene of interest that functionally complements the uninduced oncogene, and a Cre-ER system capable of excising the recombinant gene of interest. When the Cre-ER system is activated, the recombinant gene of interest is excised. From the effect on the mouse cell it is possible to determine whether the recombinant gene of interest is a tumor maintenance gene.06-25-2009
20100223678 protein isoforms of the pif-family and uses thereof - A method for screening for or diagnosis or prognosis of a neurological disorder associated with de-regulated glutamate signalling in a subject, for determining the stage or severity of such a neurological disorder in a subject, for identifying a subject at risk of developing such a neurological disorder, or for monitoring the effect of therapy administered to a subject having such a neurological disorder, said method comprising: 09-02-2010
20100223679TARGETED AND REGIONAL CELLULAR ABLATION IN ZEBRAFISH - A system including: (i) a methodology for targeted cellular ablation in zebrafish; (ii) a methodology for regional cellular ablation in zebrafish. These methodologies are used to identify genetic components that regulate cellular regeneration and to identify drug compounds that influence cellular regeneration for the purpose of developing therapies for degenerative conditions. Transgenic zebrafish disclosed herein contain transgenic constructs composed of: (i) cell and/or tissue-type specific regulatory elements (e.g. promoter and/or enhancer regions) which delimit expression of operably linked gene product(s) to discrete cellular populations; (ii) a gene product that promotes cellular ablation composed of a pro-drug conversion system capable of converting nontoxic pro-drugs into cytotoxic drugs, which is expressed alone or in connection with; (iii) a reporter gene product that allows selective detection of cells expressing the reporter—both prior to (initial cells) and following cellular ablation (regenerated cells). Here we describe genetic delivery of a pro-drug converting system in order to enable targeted cellular ablation in zebrafish, Transgenic zebrafish of this invention provide a high-throughput system for genetic dissection of the process of cellular regeneration and, compound screening for the discovery of drugs capable of promoting cellular regeneration.09-02-2010
20120144506DOUBLE-FUSION HUMAN EMBRYONIC STEM CELLS, METHOD OF MAKING DOUBLE-FUSION HUMAN EMBRYONIC STEM CELLS, TRIPLE-FUSION HUMAN EMBRYONIC STEM CELLS, METHOD OF MAKING TRIPLE-FUSION HUMAN EMBRYONIC STEM CELLS, AND METHODS OF MONITORING DOUBLE-FUSION HUMAN EMBRYONIC STEM CELLS AND TRIPLE-FUSION HUMAN EMBRYONIC STEM CELLS - Embodiments of the present disclosure include double-fusion human embryonic stem cells, methods of imaging double-fusion human embryonic stem cells, double-fusion polynucleotides, double-fusion proteins, triple-fusion human embryonic stem cells, methods of imaging triple-fusion human embryonic stem cells, triple-fusion polynucleotides, triple-fusion proteins, methods of monitoring the progression of human embryonic stem cells, methods of making isolated double-fusion human embryonic stem cells, methods of making isolated triple-fusion human embryonic stem cells, and the like.06-07-2012
20120144504CASPASE-8 AND SKIN DISEASE - The invention relates to the treatment or prevention of an inflammatory skin disease, disorder or condition, by modulating a protein that is normally regulated by caspase-8 in the skin or by increasing caspase-8 activity or level in the skin. Another aspect of the invention relates to methods for diagnosing an inflammatory skin disease, disorder or condition or a predisposition to develop said disease disorder or condition in an individual. Further aspects of the invention relate to methods for identifying target proteins involved in the course or pathology of an inflammatory skin disease, disorder or condition and to methods of screening a candidate compound for treating said disease, disorder or condition. In particular, the invention relates to inflammatory skin diseases such as atopic dermatitis and psoriasis.06-07-2012
20090113562Novel T7 Phage Peptide Display System and Uses Thereof - A bacteriophage T7 display vector for expressing and displaying an exogenous peptide, wherein the display vector comprises a polynucleotide encoding a bacteriophage T7 tail fiber protein p17 in which a hepatocyte-targeting determinant sequence is inactivated, and wherein a cloning site is contained in a coding sequence for the tail fiber protein p17 or in a coding sequence for a capsid protein p10B. Also provided are a host cell containing the display vector as described above, a bacteriophage T7 particle comprising at least one copy of a p17 protein which comprises an exogenous peptide displayed thereon, or at least one copy of a p10 protein with an exogenous peptide displayed thereon, wherein a hepatocyte-targeting determinant sequence on the bacteriophage T7 tail fiber protein p17 is inactivated. The present invention further provides a viral lysate containing assembled bacteriophage T7 particle described above, and a method for determining if a candidate peptide is a liver-targeting peptide, or for screening for liver targeting peptides.04-30-2009
20080244760Transgenic Frog Lines and Assays Employing Them - Rhodopsin transgenes driven by rhodopsin promoters were produced, some attached to GFP coding sequences as a fusion construct. When the resulting transgenes were introduced into 10-02-2008
20080244761T1R HETERO-OLIGOMERIC TASTE RECEPTORS AND CELL LINES THAT EXPRESS SAID RECEPTORS AND USE THEREOF FOR IDENTIFICATION OF TASTE COMPOUNDS - The present invention relates to the discovery that the T1R receptors assemble to form functional taste receptors. Particularly, it has been discovered that co-expression of T1R1 and T1R3 results in a taste receptor that responds to umami taste stimuli, including monosodium glutamate. Also, it has been discovered that co-expression of the T1R2 and T1R3 receptors results in a taste receptor that responds to sweet taste stimuli including naturally occurring and artificial sweeteners.10-02-2008
20110113495SCREENING METHOD FOR AGENTS SUITABLE FOR PROPHYLAXIS AND THERAPY OF ALZHEIMER'S DISEASE (AD) - Described is a method of screening for a therapeutic agent useful in the prophylaxis or treatment of AD comprising detecting oligomers of a peptide comprising an APP-G05-12-2011
20100299766MOUSE MODELS CARRYING A KNOCK-OUT MUTATION OF THE QPCTL-GENE - A knock-out non-human animal, in particular a mouse, carrying a QPCTL knock-out mutation. Additionally, respective cells and cell lines and methods and compositions for evaluating agents that affect QPCTL, for use in compositions for the treatment of QPCTL-related diseases are disclosed.11-25-2010
20100306862NON-HUMAN ANIMAL MODEL FOR FRONTOTEMPORAL LOBAR DEGENERATION WITH UBIQUITIN-POSITIVE INCLUSIONS (FTLD-U) - Non-human animal models for frontotemporal lobar degeneration with ubiquitin-positive inclusions (FTLD-U) are disclosed. The invention relates to a transgenic mouse whose genome comprises a transgene operably linked to a neuronal specific promoter effective for an increased expression of the transgene in the brain of the mouse, in which the transgene comprises a nucleotide sequence encoding TAR DNA-binding protein 43 (TDP-43). The transgenic mouse exhibits reduced or impaired learning and memory capacity, and may further exhibits progressively impaired or reduced motor functions. Methods of using such animal models are also disclosed.12-02-2010
20130133089HIGH AFFINITY LEPTINS AND LEPTIN ANTAGONISTS - Leptin muteins, in particular leptin antagonists, with increased binding affinity to leptin receptor are provided. These compounds as well as pharmaceutical composition comprising them are useful for the treatment of any disorder in which a non-desirable or deleterious activity of endogenous leptin or an altered innate immune response is implicated.05-23-2013
20100306861METHODS AND APPARATUSES FOR CONDUCTING ASSAYS IN ANIMALS - The invention provides apparatuses, systems, and methods for conducting assays in aquatic animals. The apparatuses, systems, and methods of the invention can be used to identify and/or characterize compounds that modulate morphological, anatomical, or behavioral characteristics. The apparatuses, systems, and methods of the invention can be used to identify and/or characterize compounds that modulate learning or memory.12-02-2010
20100319076TRANSGENIC NON-HUMAN ANIMALS FOR PHARMACOLOGICAL AND TOXICOLOGICAL STUDIES - The present invention is directed to the production, breeding and use of transgenic non-human animals such as mice in which specific genes or portions of genes have been replaced by homologues from another animal to make the physiology of the animals so modified more like that of the other animal with respect to drug pharmacokinetics and metabolism. The invention also extends to the use of the genetically modified non-human animals of the invention for pharmacological and/or toxicological studies.12-16-2010
20130139273Chronic Lymphocytic Leukemia Modeled in Mouse by Targeted miR-29 Expression - A mouse model and uses there of for detecting, treating, characterizing, and diagnosing various diseases are described.05-30-2013
20110010780KCNN3 AS DIAGNOSTIC AND THERAPEUTIC TARGET FOR NEURODEGENERATIVE DISEASES - The present invention discloses a dysregulation of the KCNN3 gene and the protein products thereof in Alzheimer's disease patients and individuals being at risk of developing Alzheimer's disease. Based on this finding, the invention provides methods for diagnosing and prognosticating Alzheimer's disease in a subject, and for determining whether a subject is at increased risk of developing Alzheimer's disease. Furthermore, this invention provides therapeutic and prophylactic methods for treating and preventing Alzheimer's disease and related neurodegenerative disorders using the KCNN3 gene and its corresponding gene products. Screening methods for modulating agents of neurodegenerative diseases are also disclosed.01-13-2011
20110016543GENOMIC EDITING OF GENES INVOLVED IN INFLAMMATION - The present invention provides genetically modified animals and cells comprising edited chromosomal sequences encoding inflammation-related proteins. In particular, the animals or cells are generated using a zinc finger nuclease-mediated editing process. Also provided are methods of assessing the effects of agents in genetically modified animals and cells comprising edited chromosomal sequences encoding inflammation-related proteins.01-20-2011
20110023149GENOMIC EDITING OF GENES INVOLVED IN TUMOR SUPPRESSION IN ANIMALS - The present invention provides genetically modified animals and cells comprising edited chromosomal sequences involved in tumor suppression. In particular, the animals or cells are generated using a zinc finger nuclease-mediated editing process. The invention also provides zinc finger nucleases that target chromosomal sequence involved in tumor suppression and the nucleic acids encoding the zinc finger nucleases. Also provided are methods of assessing the effects of agents in genetically modified animals and cells comprising edited chromosomal sequences involved in tumor suppression.01-27-2011
20100333216Non-human gene-disrupted animal with disrupted Adam11 gene - It is an object of the present invention to provide a non-human gene-disrupted animal with a disrupted ADAM11 gene. According to the present invention, a non-human gene-disrupted animal, wherein either one of or both alleles of an ADAM11 gene are disrupted, is provided.12-30-2010
20110030070DIAGNOSIS AND TREATMENT OF AUTISM USING CD38 - The invention relates to a method for screening a pharmaceutical for treating or preventing a neurodevelopmental disorder or a psychiatric disorder accompanied by an abnormality of oxytocin system by using an increase in expression or enzymatic activity of CD38 as an index, and a diagnosis of a predisposition to a neurodevelopmental disorder or a psychiatric disorder accompanied by an abnormality of oxytocin system by using a mutation present in a CD38 gene region as an index.02-03-2011
20110030071Transgenic Animal Model of Cancer and Methods of Use - The invention features a transgenic mouse model of cancer, exemplified by basal cell carcinoma, which finds use in identification of anti-cancer drugs. The transgenic mouse is characterized by a heterozygous defect in a Patch gene (Ptch02-03-2011
20110035816Genetically Modified Rat Models for Drug Metabolism - The present invention provides a desired rat or a rat cell which contains a predefined, specific and desired alteration rendering the rat or rat cell predisposed to alterations in drug and chemical metabolism by modification of its structure or mechanism. Specifically, the invention pertains to a genetically altered rat, or a rat cell in culture, that is defective in at least one of two alleles of a drug metabolism gene such as the Cyp7b1 gene, the Cyp3a4 gene, etc. In another embodiment, the rat cell is a somatic cell. The inactivation of at least one drug metabolism allele results in an animal with a higher susceptibility to altered drug and chemical metabolism. In one embodiment, the genetically altered animal is a rat of this type and is able to serve as a useful model for altered drug and chemical metabolism or toxicology and as a test animal for autoimmune and other studies. The invention additionally pertains to the use of such rats or rat cells, and their progeny in research and medicine. In one embodiment, the invention provides a genetically modified or chimeric rat cell whose genome comprises two chromosomal alleles of a drug metabolism gene wherein at least one of the two alleles contains a mutation, or the progeny of the cell.02-10-2011
20110041191Animal model, and products and methods useful for the production thereof - The present invention relates to a transgenic animal suitable for modelling Alzheimer's Disease. The present invention also relates to cells and gametes of the transgenic animal of the invention, along with nucleic acids and vectors suitable for generating the transgenic animal. Methods of generating the transgenic animal are also described, along with screening methods utilizing the transgenic animal.02-17-2011
20110041190NOVEL CHIMERIC PROTEINS - Novel chimeric proteins are disclosed. The proteins comprise at least two portions. The first portion binds to a first cell and decreases the cell's ability to send a trans signal to a second cell; the second portion sends its own trans signal to the second cell. Methods for making and using these proteins in the treatment of cancer, viral infections, autoimmune and alloimmune diseases are also disclosed, as are pharmaceutical formulations comprising the novel chimeric proteins and genes. Either the proteins themselves or a genetic sequence encoding the protein can be administered. Other methods are also disclosed in which two molecular components result in decrement of a first trans signal from a first cell and the conferring of a second trans signal to a second cell.02-17-2011
20110041192RECOMBINANT NON-HUMAN MAMMALIAN MODEL FOR HEPATITIS INFECTION AND IMMUNOPATHOGENESIS - Provided herein is a recombinant non-human mammal having an immune system including human immune cells and having a liver including human liver cells, and methods for producing the same. Also provided are methods of screening a compound for activity in treating hepatitis, comprising: administering a test compound to a recombinant non-human mammal as described herein; and then detecting the presence or absence of said activity in said mammal (e.g., by biochemical assay), said presence of said activity in said mammal indicating that said compound has activity in treating hepatitis. Methods of making fusion cells useful for the production of human monoclonal antibodies are also provided.02-17-2011
20090172826Model System for TCR (ZETA) Chain Downregulation - The present invention refers to an animal model system which mimics the immunosuppressive environment found in cancer, autoimmune and infectious diseases, as well as in chronic inflammation. In said animal model system, which is an object of the present invention, sustained exposure to antigen induces TCR ζ chain downregulation and impaired T cell function. Further objects of the present invention are the method of generating the animal model system, as well as methods of screening for substances that inhibit said ζ chain downregulation. Finally, the present invention provides ζ chain as a marker for the immunological status of a subject in need of immunotherapy.07-02-2009
20090178146Regulators of NFAT - Disclosed are methods of identifying an agent that modulates an NFAT regulator protein. One such method comprises contacting at least one test agent with a recombinant cell comprising at least one NFAT regulator protein or fragment or derivative thereof, assessing the effect of the test agent on an activity, interaction, expression, or binding to the NFAT regulator protein or fragment or derivative thereof, and identifying the test agent that has an effect on an activity, interaction, expression, or binding to the NFAT regulator protein or fragment or derivative thereof, whereby the identified test agent is characterized as an agent that modulates an NFAT regulator protein. Methods of identifying an agent that modulates intracellular calcium, methods to screen for an agent that modulates NFAT regulator function, methods to diagnose unexplained immunodeficiency in a subject, and methods for identifying an agent for treating or preventing a disease or disorder associated with a NFAT regulator protein or calcium signaling are also disclosed.07-09-2009
20100146643RAPID IN VIVO MODEL FOR ANGIOGENESIS - An animal model of angiogenesis is described. Nascent blood vessels are supported by a growth matrix comprising a growth factor. The nascent blood vessels are labeled with a fluorescent protein selectively expressed in cells forming these vessels.06-10-2010
20090083865Transgenic Mouse Lines Expressing Human Ace2 and Uses Thereof - Animal models for severe acute respiratory syndrome-coronavirus infection of humans are needed to elucidate SARS pathogenesis and develop vaccines and antivirals. Transgenic mice were developed expressing human angiotensin-converting enzyme 2, a functional receptor for the virus, under the regulation of a global promoter. A transgenic lineage, designated AC70, was among the best characterized against SARS coronavirus infection, showing weight loss and other clinical manifestations before reaching 100% mortality within 8 days after intranasal infection. Inflammatory mediators were also detected in these tissues, coinciding with high levels of virus replication. In contrast, infected transgene-negative mice survived without showing any clinical illness. The severity of the disease developed in these transgenic mice, AC70 in particular, makes these mouse models valuable not only for evaluating the efficacy of antivirals and vaccines, but also for studying SARS coronavirus pathogenesis and infection by other coronaviruses utilizing human ACE2 for viral entry into cells.03-26-2009
20110214189G PROTEIN COUPLED RECEPTORS AND USES THEREOF - The present invention provides GPCR polypeptides and polynucleotides, recombinant materials, and transgenic mice, as well as methods for their production. The polypeptides and polynucleotides are useful, for example, in methods of diagnosis and treatment of diseases and disorders. The invention also provides methods for identifying compounds (e.g., agonists or antagonists) using the GPCR polypeptides and polynucleotides of the invention, and for treating conditions associated with GPCR dysfunction with the GPCR polypeptides, polynucleotides, or identified compounds. The invention also provides diagnostic assays for detecting diseases or disorders associated with inappropriate GPCR activity or levels.09-01-2011
20110214191METHOD FOR THE IDENTIFICATION OF GENES INVOLVED IN NEURODEGENERATIVE PROCESSES - A method for the identification of genes involved in neurodegenerative processes, detectable by the late onset of a phenotype associated with neurodegeneration, by means of a genetic screen of deregulated genes, which comprises the measurement of sleep-wake cycle activity schemes in different stages of life, young and adult, of individuals of an animal model, such as 09-01-2011
20110214190TRANSGENIC REPORTER MOUSE AND METHOD FOR USE - A transgenic mammal, including a transgenic mouse, whose genome comprises a transgene, said transgene comprises a neutrophil gelatinase-associated lipocalin (NGAL) promoter gene operably linked to at least one sequence encoding at least one of a fluorescent or bioluminescent protein, wherein the NGAL promoter gene expression in the mouse can be assayed by bioluminescence or fluorescence imaging.09-01-2011
20100146645TRANSGENIC ANIMAL MODEL FOR MODELLING PATHOLOGICAL ANXIETY, A METHOD FOR IDENTIFYING COMPOUNDS FOR TREATMENT OF DISEASES OR DISORDERS CAUSED BY PATHOLOGICAL ANXIETY AND A METHOD FOR USING WFS1 PROTEIN AS A TARGET FOR IDENTIFYING EFFECTIVE COMPOUNDS AGAINST PATHOLOGICAL ANXIETY - The invention discloses the transgenic animal model for pathological anxiety, the method to generate this model, the method to test drugs and drug candidates for the treatment of pathological anxiety and the method to use Wfs1 as target for screening of new anxiolytic drugs to treat pathological anxiety. This animal model is useful to test potential drug candidates for the treatment of diseases caused by pathological anxiety and to screen therapeutic compounds for the psychiatric disorders caused by reduces stress-tolerance and deficiency in adaptation to environmental challenges.06-10-2010
20110126299TRIPLE TRANSGENIC MOUSE MODEL OF AUTOIMMUNE DISEASE AND NF-KAPPA B IN VIVO IMAGING - The present invention provides for monitoring of NF-κB-associated inflammation in mice undergoing Id-driven autoimmune disease. The mice are triple transgenic mice expressing both Id05-26-2011
20110126298Transgenic Mice Over-Expressing Receptor For Advanced Glycation Endproduct (RAGE) In Brain And Uses Thereof - The present invention provides for a transgenic non-human animal whose cells contain a DNA sequence comprising: (a) a nerve tissue specific promoter; and (b) a DNA sequence which encodes a receptor for advanced glycation endproducts (RAGE), wherein the promoter and the DNA sequence which encodes the receptor for advanced glycation endproducts (RAGE) are operatively linked to each other and integrated in the genome of the non-human animal, and wherein said non-human animal exhibits a reduced amount of cerebral tissue infarcted following a transient middle cerebral artery occlusion compared to an identical non-human animal lacking said DNA sequence.05-26-2011
20110126297TRANSGENIC ANIMAL WITH MONOCYTE CHEMOTACTIC PROTEIN 1 PROMOTER - The present invention relates to a transgenic animal, which comprises in its genome a recombinant polynucleotide encoding one or more reporter proteins and a monocyte chemotactic protein-1 (MCP-1) promoter, wherein the one or more reporter proteins are expressed under the control of the MCP-1 promoter. A method for monitoring endogenous expression of MCP-1 in vivo is also provided, which is useful for identifying a regulator of the expression of MCP-1 or an anti-inflammatory agent.05-26-2011
20100132057GENETICALLY MODIFIED ANIMAL FOR USE IN EVALUATING HARMFULNESS OF TEST SUBSTANCE - A genetically modified animal that includes an introduced DNA including a functionally linked aryl hydrocarbon receptor-binding enhancer located 5′-upstream of a tyrosine hydroxylase gene, promoter of any type, reporter gene, and poly(A) addition signal.05-27-2010
20100132055ANIMAL MODEL FOR THE SELECTION AND VALIDATION OF AGENTS ACTIVE AGAINST PULMONARY EMPHYSEMA AND COLORECTAL CANCER - The present invention relates to a non-human animal model, cell and tissue cultures derived therefrom, which do not produce or produce only suboptimal levels of one or more functional sestrins and in addition do not produce or do only produce suboptimal levels of latent transforming growth factor β binding protein 4 (ltbp4). Furthermore, the present invention relates to a method for selecting agents for treating the pulmonary emphysema and/or the colorectal cancer exhibited by utilizing the animal model, cell or tissue culture of the invention. The animal model, cell or tissue culture is suitable for preclinical testing of efficacy, toxicity and bioavailability of potential agents.05-27-2010
20120036587PROSTATE CANCER CELL LINES AND THEIR USE IN SCREENING METHOD - The present invention relates to a prostate cancer cell line CNCM deposit number I-4126, the use thereof for preparing resistant prostate cancer cell lines, the resistant prostate cancer cell lines, and the use of these prostate cancer cell lines for screening compounds of interest.02-09-2012
20090031436Compositions and Methods Relating to Cornelia De Lange Syndrome - Animal models, kits, and methods for diagnosis and treatment of Cornelia de Lange Syndrome are disclosed. In especially preferred aspects, altered gene expression of selected genes is correlated with a NIPBL+/− genotype to thereby identify surrogate markers, which may then be used to diagnose Cornelia de Lange Syndrome.01-29-2009
20090031435SMA Therapy and Cell Based Assay - This invention relates to therapies for diseases involving splicing defects, such as spinal muscular atrophy (SMA), and methods to identify compounds for treating this disease. The invention specifically provides for therapies comprised of small molecule compounds identified by cell-based high-throughput screening assays. These assays utilize engineered splicing constructs that fuse pre-mRNA fragments to a reporter gene. The fragments contain exons and at least one intron of a gene mutated in such a way to cause disease. Additionally, the invention provides for methods to monitor the effects of drugs on splicing and gene expression in vivo, in transgenic animals.01-29-2009
20100017894Mutants of Human App and Their Use for the Production of Transgenice Animals - A modified amyloid precursor protein can be expressed from a DNA construct comprising an APP DNA sequence, or a fragment or artificial substrate thereof, encoding the mutation I45W, I45Y V46W or V46Y (numbering relative to A4CT); the use of the DNA construct in the generation of cell lines or transgenic animals and the use of these proteins or such transgenic animals in the diagnosis of Alzheimer's Disease and screening putative drugs against Alzheimer's Disease are also described.01-21-2010
20100017897PRRG4-ASSOCIATED COMPOSITIONS AND METHODS OF USE THEREOF IN METHODS OF TUMOR DIAGNOSIS - Compositions and methods for detecting PRRG4- and PRRG2 associated molecules are provided as are methods of use thereof for the detection and treatment of cancer.01-21-2010
20090313709Genetically Modified Animal and Use Thereof - The present invention provides a transgenic mouse retaining a DNA that encodes an exogenous GPR40 in an expressible state, wherein (1) the insulin secretion capacity has been increased, and/or (2) the glucose tolerance has been improved, compared with the corresponding non-transgenic mouse, or a portion of the living body thereof, a screening method for a prophylactic/therapeutic drug for diabetes mellitus and metabolic syndrome using the transgenic mouse, and the like.12-17-2009
20090313707Novel Gene Disruptions, Compositions and Methods Relating Thereto - The present invention relates to transgenic animals, as well as compositions and methods relating to the characterization of gene function. Specifically, the present invention provides transgenic mice comprising disruptions in PRO69122, PRO204, PRO214, PRO222, PRO234, PRO265, PRO309, PRO332, PRO342, PRO356, PRO540, PRO618, PRO944, PRO994, PRO1079, PRO1110, PRO1122, PRO1138, PRO1190, PRO1272, PRO1286, PRO1295, PRO1309, PRO1316, PRO1383, PRO1384, PRO1431, PRO1434, PRO1475, PRO1481, PRO1568, PRO1573, PRO1599, PRO1604, PRO1605, PRO1693, PRO1753, PRO1755, PRO1777, PRO1788, PRO1864, PRO1925, PRO1926, PRO3566, PRO4330, PRO4423, PRO36935, PRO4977, PRO4979, PRO4980, PRO4981, PRO5801, PRO5995, PRO6001, PRO6095, PRO6182, PRO7170, PRO7171, PRO7436, PRO9912, PRO9917, PRO37337, PRO37496, PRO19646, PRO21718, PRO19820, PRO21201, PRO20026, PRO20110, PRO23203 or PRO35250 genes. Such in vivo studies and characterizations may provide valuable identification and discovery of therapeutics and/or treatments useful in the prevention, amelioration or correction of diseases or dysfunctions associated with gene disruptions such as neurological disorders; cardiovascular, endothelial or angiogenic disorders; eye abnormalities; immunological disorders; oncological disorders; bone metabolic abnormalities or disorders; lipid metabolic disorders; or developmental abnormalities.12-17-2009
20090313708GPR22 AND METHODS RELATING THERETO - Methods for generating an expression-enhanced GPR22 nucleic acid, as well as substituted GPR22 nucleic acids providing for enhanced expression of the encoded GPR22 polypeptide, are provided. In practicing the subject methods, a nucleic acid encoding a mammalian GPR22 receptor polypeptide (e.g., a wild-type nucleic acid) is expression-enhanced by identifying the various codons of the coding region for the GPR22 amino acid sequence and substituting nucleotides so as to enhance expression without changing the amino acid sequence of the encoded GPR22 polypeptide. Methods, compositions, and kits using the same for screening of modulators of GPR22 are also provided.12-17-2009
20100011452CHIMERIC NON-HUMAN ANIMAL - The present invention relates to a method for producing a chimeric non-human animal expressing a desired protein, and a chimeric non-human animal or an offspring thereof expressing a desired protein.01-14-2010
20090217391T1R3 A NOVEL TASTE RECEPTOR - The present invention relates to the discovery, identification and characterization of a receptor protein, referred to herein as T1R3, which is expressed in taste receptor cells and associated with the perception of bitter and sweet taste. The invention encompasses T1R3 nucleotides, host cell expression systems, T1R3 proteins, fusion protein, transgenic animals that express a T1R3 transgene, and recombinant “knock-out” animals that do not express T1R3. The invention further relates to methods for identifying modulators of the T1R3-mediated taste response and the use of such modulators to either inhibit or promote the perception of bitterness or sweetness. The modulators of T1R3 activity may be used as flavor enhancers in food, beverages and pharmaceuticals.08-27-2009
20090217390Non-human animal sarcoma model - The invention disclosed in this application relates to a method designed to obtain a non-human animal model for sarcoma characterised in that it comprises: transfecting cells derived from a multipotent mesenchymal cell line with an expression vector that contains a polynucleotide which encodes a fusion protein selected from EWS-FLI1, EWS-ERG, EWS-ETV1, EWS-ETV4, EWS-FEV, EWS-ATF1, EWS-WT1, EWS-NR4A3 and EWS-DDIT3; and injecting said transfected cells in the animal that is the model subject. Similarly, this invention relates to the animal model itself and its applications, as well as the transfected cell line and the applications thereof.08-27-2009
20110093960Methods of identifying agents that ameliorate or modulate effects of PRO1328 gene disruptions - The present invention relates to transgenic animals, as well as compositions and methods relating to the characterization of gene function. Specifically, the present invention provides transgenic mice comprising disruptions in PRO227, PRO233, PRO238, PRO1328, PRO4342, PRO7423, PRO10096, PRO21384, PRO353 or PRO1885 genes. Such in vivo studies and characterizations may provide valuable identification and discovery of therapeutics and/or treatments useful in the prevention, amelioration or correction of diseases or dysfunctions associated with gene disruptions such as neurological disorders; cardiovascular, endothelial or angiogenic disorders; eye abnormalities; immunological disorders; oncological disorders; bone metabolic abnormalities or disorders; lipid metabolic disorders; or developmental abnormalities.04-21-2011
20100071078RSPONDINS AS MODULATORS OF ANGIOGENESIS AND VASCULOGENESIS - The present invention relates to the use of Rspondins, particularly Rspondin2 (Rspo2) or Rspondin3 (Rspo3) or Rspondin nucleic acids, or regulators or effectors or modulators of Rspondin, e.g. Rspo2 and/or Rspo3 to promote or inhibit angiogenesis and/or vasculogenesis, respectively. The invention is based on the demonstration that Rspo3 and Rspo2 are angiogenesis promoters, and the identification of Rspo2 and 3 as positive regulators of vascular endothelial growth factor (VEGF). These results indicate a major role for Rspondins, particularly Rspo3 and/or Rspo2 in the signaling system during angiogenesis. The invention also relates to the use of regulators or effectors or modulators of Rspondin3, including agonists and antagonists, in the treatment of conditions where treatment involves inhibiting or promoting angiogenesis and/or vasculogenesis.03-18-2010
20110083199Non-Human Animal Model for Cardiovascular Disease Characterized by a Disrupted Fibulin-4 Gene - The invention relates to an animal model of cardiovascular disease and a method of preparation and use thereof. In particular, it relates to a genetically engineered animal model of aortic aneurysms and methods for screening drugs using the animal model. Provided is a genetically-modified, non-human mammal, wherein the modification results in a disrupted Fibulin-4 gene. Also provided is a genetically-modified animal cell containing a disrupted Fibulin-4 gene. The mammal or animal cell can be used as a model for a cardiovascular condition or disease, preferably aortic aneurysm, more preferably thoracic aortic aneurysm. Furthermore, methods for identify or validating a compound that can be used to treat or to prevent an aberrant cardiovascular condition are provided, as well as method to identify a gene involved in the response to aortic failure.04-07-2011
20110252485Novel gene disruptions, compositions and methods relating thereto - The present invention relates to transgenic animals, as well as compositions and methods relating to the characterization of gene function. Specifically, the present invention provides transgenic mice comprising disruptions in PRO844, PRO1131 or PRO5992 genes. Such in vivo studies and characterizations may provide valuable identification and discovery of therapeutics and/or treatments useful in the prevention, amelioration or correction of diseases or dysfunctions associated with gene disruptions such as neurological disorders; cardiovascular, endothelial or angiogenic disorders; eye abnormalities; immunological disorders; oncological disorders; bone metabolic abnormalities or disorders; lipid metabolic disorders; or developmental abnormalities.10-13-2011
20110093959 CRYPTOTIS PARVA SCREENING MODEL FOR ANTIEMETIC POTENTIAL - The present invention provides for anrelate to an animal model for characterizing emesis, and for screening and characterizing emetic and antiemetic agents. In several embodiments, the Least Shrew, 04-21-2011
20120174240ROLE OF PROTEOGLYCANS IN DRUG DEPENDENCE - The invention provides methods of preventing or treating drug addiction, or ameliorating the craving for an addictive drug, as well as compounds, peptides, and pharmaceutical compositions that may be used to prevent or treat drug addiction or ameliorate the craving for an addictive drug. The invention also provides methods for identifying agents that may be used to prevent or treat drug addiction, or ameliorate the craving for an addictive drug.07-05-2012
20120304318CANCER DIAGNOSIS AND TREATMENT - The invention concerns materials and methods relating to the use of OMD (osteomodulin) and\or PRELP (Proline/arginine-rich end leucine-rich repeat protein) expression, particularly under-expression, to discriminate cancer and non-cancer cells in a variety of cancers. The invention further provides methods and materials based on OMD and\or PRELP for use in therapy e.g. to suppress cancer initiation or development.11-29-2012
20120304317TRANSGENIC RODENT EXPRESSING TRUNCATED DISC1 - The invention provides transgenic rodents, particularly mice, expressing truncated versions of the Disrupted-in-Schizophrenia-1 (DISC1) gene and showing Schizophrenia-related neural and behavioral phenotypes. The rodents of the invention have (1) a plurality of copies of a heterologous truncated Disc1 genomic DNA sequence which includes at least 1 stop codon after exon 8 such as to encode a Disc1 polypeptide truncated before exon 9; (2) 2 copies of endogenous Disc1 genomic DNA sequence encoding full length Disc1 polypeptide. Also provided are related materials and methods.11-29-2012
20110088102METHODS OF IDENTIFYING INHIBITORS OF GENE SILENCING IN MAMMALIAN CELLS - Disclosed herein are methods of identifying inhibitors of gene silencing or re-silencing, which can include repressing expression of a selectable marker gene in mammalian cells, treating the cells with at least one test compound, growing the cells under selective conditions, and quantifying the relative number of cells that live, wherein a change in the relative number of cells as compared to cells that were not treated with the test compound, identifies the compound as an inhibitor of gene silencing or re-silencing. Also disclosed herein are transgenic mice and isolated cell lines that are useful in the disclosed methods and kits for use in performing the disclosed methods.04-14-2011
20110083200Method For Testing Efficacy Of Treatment Of Neurologic Disorders - The method of the invention is useful for evaluating pharmaceutical compositions for treatment of neurological diseases encompassing neurological or neurodegenerative diseases associated with cognitive dysfunction and, in particular, dementia; schizophrenia; anxiety; depression; and pain using a rodent behavioral assay, wherein the method is useful in testing compositions useful in the modulation, amelioration, prevention, or treatment of dementia using a non-human animal carrying at least a transgene for human amyloid-beta protein or human tau and transgenes causing the elevated production of the human amyloid-beta protein in the animal as compared to nontrans genie animals of the same genetic background and the behavior is a nesting behavior.04-07-2011
20110107439DIAGNOSTIC OF PRE-SYMPTOMATIC METABOLIC SYNDROME - The invention relates to a method for diagnosing pre-symptomatic metabolic syndrome in a subject, wherein said method comprises determining the expression level of a gene represented by a sequence selected from the group consisting of SEQ ID NO: 1-18 in a subject. The invention described target genes for preventing or stopping further progress of metabolic syndrome into clinical disease states.05-05-2011
20120073001METHODS AND COMPOSITIONS FOR TREATING OR PREVENTING PRURITIS - The invention features therapeutic compositions comprising agents useful for the treatment or prevention of pruritis, and methods useful for identifying such agents.03-22-2012
20110061114NOVEL PRO258 GENE DISRUPTIONS, AND METHODS RELATING THERETO - The present invention relates to transgenic animals, as well as compositions and methods relating to the characterization of gene function. Specifically, the present invention provides transgenic mice comprising disruptions in PRO196, PRO217, PRO231, PRO236, PRO245, PRO246, PRO258, PRO287, PRO328, PRO344, PRO357, PRO526, PRO724, PRO731, PRO732, PRO1003, PRO1104, PRO1151, PRO1244, PRO1298, PRO1313, PRO1570, PRO1886, PRO1891, PRO4409, PRO5725, PRO5994, PRO6097, PRO7425, PRO10102, PRO10282, PRO61709 or PRO779 genes. Such in vivo studies and characterizations may provide valuable identification and discovery of therapeutics and/or treatments useful in the prevention, amelioration or correction of diseases or dysfunctions associated with gene disruptions such as neurological disorders; cardiovascular, endothelial or angiogenic disorders; eye abnormalities; immunological disorders; oncological disorders; bone metabolic abnormalities or disorders; lipid metabolic disorders; or developmental abnormalities.03-10-2011
20110035815Mosaic knockout mouse tumor models and methods or use - Disclosed herein are transgenic mouse tumor models. A portion of the cells of the disclosed transgenic mice undergo directed somatic recombination and the mouse is therefore a mosaic for homozygous knockout of p53, NF1, or both p53 and NF1 genes. The homozygous null cells resulting from the somatic recombination also express a detectable fluorescent protein, and the resulting sibling cells, which are wild type for p53, NF1, or both p53 and NF1, express a different detectable fluorescent protein. Also disclosed herein are methods of identifying compounds for treating or preventing a tumor, using the disclosed transgenic mice.02-10-2011
20110030072GENOME EDITING OF IMMUNODEFICIENCY GENES IN ANIMALS - The present invention provides genetically modified animals and cells comprising edited chromosomal sequences encoding immunodeficiency proteins. In particular, the animals or cells are generated using a zinc finger nuclease-mediated editing process. Also provided are methods of assessing the effects of agents in genetically modified animals and cells comprising edited chromosomal sequences encoding immunodeficiency proteins.02-03-2011
20100325743Marks as modifiers of the p53 pathway and methods of use - Human MARK genes are identified as modulators of the p53 pathway, and thus are therapeutic targets for disorders associated with defective p53 function. Methods for identifying modulators of p53, comprising screening for agents that modulate the activity of MARK are provided.12-23-2010
20130160150METHODS FOR IDENTIFYING COMPOUNDS THAT MODULATE LISCH-LIKE PROTEIN OR C1ORF32 PROTEIN ACTIVITY AND METHODS OF USE - The invention provides methods for reducing diabetes susceptibility in a subject and methods for increasing the expression of LL or CLORF32 in a subject. The invention further provides a method for identifying an agent which modulates expression of an Ll RNA or Clorf32 RNA comprising contacting a cell with an agent; determining expression of the Ll RNA or Clorf32 RNA in the presence and the absence of the agent; and comparing expression of the Ll RNA or Clorf32 RNA in the presence and the absence of the agent, wherein a change in the expression of the Ll RNA or Clorf32 RNA in the presence of the agent is indicative of an agent which modulates the level of expression of the RNA.06-20-2013
20110154512Humanized Fc gamma R Mice - Genetically modified non-human animals and methods and compositions for making and using them are provided, wherein the genetic modification comprises a deletion of the endogenous low affinity FcγR locus, and wherein the mouse is capable of expressing a functional FcRγ-chain. Genetically modified mice are described, including mice that express low affinity human FcγR genes from the endogenous FcγR locus, and wherein the mice comprise a functional FcRγ-chain. Genetically modified mice that express up to five low affinity human FcγR genes on accessory cells of the host immune system are provided.06-23-2011
20110154510AUTOMATED HIGH-CONTENT LIVE ANIMAL DRUG SCREENING USING C. ELEGANS - The present invention relates to methods and compositions for high content drug screening in 06-23-2011
20110154511HEPARANASE DEFICIENT NON-HUMAN MAMMALS - The invention relates to cells and transgenic non-human mammals having at least one disrupted heparanase allele. The invention further relates to methods of screening therapeutic drug candidates utilizing the heparanase deficient non-human mammals and cells.06-23-2011
20100281547Selecting animals for desired genotypic or potential phenotypic properties - Described are methods to select animals, such as mammals, particularly domestic animals, breeding animals or animals destined for slaughter, for having desired genotypic or potential phenotypic properties, in particular, related to muscle mass and/or fat deposition lean meat, lean back fat, sow prolificacy and/or sow longevity. Provided is a method for selecting an animal having desired genotypic or potential phenotypic properties comprising testing the animal, a parent of the animal or its progeny for the presence of a nucleic acid modification affecting the activity of an evolutionary conserved CpG island, located in intron 3 of an IGF2 gene and/or for the presence of a nucleic acid modification affecting binding of a nuclear factor to an IGF2 gene.11-04-2010
20120204276METHODS RELATED TO A MUTATION IN COMPLEMENT FACTOR H-RELATED PROTEIN 5 IN PATIENTS WITH GLOMERULONEPHRITIS - The invention relates to methods of regulating complement. In particular, the inventors have identified a relationship between a particular gene, CFHR5, and irregularities in complement regulation. The invention provides a method for diagnosing a complement related disease, comprising identifying a mutation in the CFHR5 gene in a sample obtained from a subject.08-09-2012
20080229435Mapks as Modifiers of the Rac, Axin, and Beta-Catenin Pathways and Methods of Use - Human MAPK genes are identified as modulators of the Rac, axin, and beta-catenin pathways, and thus are therapeutic targets for disorders associated with defective Rac, axin, and beta-catenin function. Methods for identifying modulators of Rac, axin, and beta-catenin, comprising screening for agents that modulate the activity of MAPK are provided.09-18-2008
20100077493GENES AND PATHWAYS INVOLVED IN BIPOLAR DISORDER - Transgenic non-human mammals and cells having a disruption in at least one allele of nArgBP2 are provided. Methods of identifying therapeutic agents for the treatment of a disorder associated with altered expression of nArgBP2 are also provided. Methods of assessing the risk of an individual developing a disorder associated with disruption of nArgBP2 and methods of treating individuals with such a disorder are provided.03-25-2010
20120204275APOE IMMUNOTHERAPY - The present invention provides antibodies that preferentially bind to an ApoE(1-272) fragment relative to ApoE(1-299). These antibodies serve to reduce the toxicity of this fragment and find use in treatment and prophylaxis of a variety of neurological diseases.08-09-2012
20120204274BITRANSGENIC MURINE MODEL FOR STUDYING MYELOPOIESIS, IMMUNITY AND TUMORIGENESIS - A myeloid-specific c-fms-rtTA/(TetO)08-09-2012
20120204273COMPOSITIONS RELATING TO A PHOSPHOPROTEIN AND METHODS OF USE - The invention provides methods and compositions for identifying agents that modulates 138-kDa C2 domain-containing phosphoprotein (CDP138) activity or phosphorylation levels both in vivo and in vitro. Also provided are methods and compositions to prolong the survival of neuronal cells, to ameliorate or prevent a condition associated with release of insulin from insulin producing cells and insulin-stimulated glucose metabolism, to inhibiting proliferation of a cancer cell and to inducing cell cycle arrest of a cancer cell.08-09-2012
20090260092METHODS OF DIAGNOSING ALZHEIMER'S DISEASE AND MARKERS IDENTIFIED BY SET ASSOCIATION - The present disclosure relates to genetic markers and methods of diagnosing and screening for late-onset Alzheimer's disease (LOAD). As such, the disclosure encompasses a whole-genome association analysis of single nucleotide polymorphisms (SNPs) of which a number are located within the GRB2-associated binding protein 2 (GAB2) gene as well as other markers associated with other genes. The disclosure identifies two novel haplotypes within the GAB2 gene, i.e., a LOAD risk-enhancing and a LOAD risk-decreasing haplotype. These haplotypes modify LOAD risk differentially in combination with APOE alleles. Further encompassed are therapeutic methods and agents of decreasing the deterioration of cells associated with LOAD.10-15-2009
20090260090APOBEC3 MEDIATED DNA EDITING - The present invention relates to methods and compositions for preventing the occurance or progression of a cancer or pre-cancerous condition associated with expression, or over-expression of human cytidine deaminases of the APOBEC3 family. The invention also relates to drug screening assays designed to identify compounds that regulate the activity, or level of expression, of hA3A, hA3C and hA3H. The invention further relates to transgenic mice, as well as cells derived from said mice, that have been genetically engineered to express, or over-express hA3A, hA3C and/or hA3H. Such mice may be utilized to screen for, or identify, compounds that modulate the activity, or expression, of the human cytidine deaminases. The present invention also provides topical compositons such as cosmetic lotion, crème, or sunscreen for use on the skin, which comprise one or more inhibitors of human cytidine deaminase activity. The present invention relates to a double stranded DNA obtained following opening up of its duplex structure, said DNA being edited with cellular protein normally or abnormally expressed in the nucleus of an eukaryotic cell. The mono stranded DNA derived from the said double stranded DNA is a part of the present invention.10-15-2009
20090241204TRANSGENIC NON-HUMAN ANIMALS FOR PHARMACOLOGICAL AND TOXICOLOGICAL STUDIES - The present invention is directed to the production, breeding and use of transgenic non-human animals such as mice in which specific genes or portions of genes have been replaced by homologues from another animal to make the physiology of the animals so modified more like that of the other animal with respect to drug pharmacokinetics and metabolism. The invention also extends to the use of the genetically modified non-human animals of the invention for pharmacological and/or toxicological studies.09-24-2009
20090241203Transgenic animal models of disease - The present invention provides transgenic, large non-human animal models of diseases and conditions, as well as methods of making and using such animal models in the identification and characterization of therapies for the diseases and conditions.09-24-2009
20090241202DOMAIN-GRAFTED ANTIBODIES - The present invention relates to antibodies. Specifically, the present invention relates to antibodies composed of novel combinations of inter-species antibody domains (“domain-grafted antibodies”). The present invention further relates to compositions comprising such domain-grafted antibodies, as well as methods for producing such domain-grafted antibodies. Finally, the present invention relates to methods of evaluating the in vivo biological effect of such domain-grafted antibodies as well as uses of such domain-grafted antibodies for cross-species evaluation of the in vivo activity antibodies intended for human therapy.09-24-2009
20110162092COMPOSITION COMPRISED OF AKAP12 AND USES OF AKAP12 MUTANT ZEBRAFISH AS AN ANIMAL MODEL - The present invention relates to a composition comprised of AKAP12 (A-Kinase anchoring protein 12) and to uses of AKAP12 mutant zebrafish as an animal model. More particularly, the following characteristics are noted in the present AKAP12 mRNA knockdown zebrafish: crooked or shortened tail, inability to move normally, non-uniform micro-vasculature in the brain, and change in heart shape with non-uniform and weak heartbeats. It also has various circulatory and genetic defects, such as hemorrhage from the ventricles of the heart, brain, and retina. All of these defects can be cured with AKAP12 injection. Therefore, AKAP12 can be used as an active component for a composition to prevent and heal circulatory and genetic defects that are caused by AKAP12 deficiency, and as a hemorrhage inhibitor. Further, the AKAP12 deficient mutant zebrafish can be useful as an animal model for verification of effectiveness of treatment for genetic defects in the circulatory system.06-30-2011
20090126031MICE LACKING ALPHA 1G SHOWING ENHANCED NOVELTY-SEEKING AND ALCOHOL PREFERENCE AND THERAPEUTIC METHODS FOR MOOD DISORDERS BY MODULATING ALPHA 1G T-TYPE CALCIUM CHANNELS - The present invention relates to a novel use of an α1G T-type calcium channel transgenic mouse as a nervous disease model, more particularly, a novel use of a mouse deficient in α1G T-type calcium channel showing novelty-seeking and alcohol preference as a nervous disease model for human nervous related diseases such as novelty-seeking character, alcoholism, anxiety and emotion disorder by stress, etc. The α1G T-type channel transgenic mice showing novelty-seeking and alcohol preference of the present invention can be effectively used for the development of a medicine and a therapeutic method for human nervous diseases.05-14-2009
20080313750Transgenic Non-Human Animal Model of Lung Tumorigenesis - The present invention is a transgenic non-human animal whose genome contains a transgene containing a nucleic acid encoding a cyclin E protein operably linked to a regulatory element including a lung-specific promoter. The transgenic animals of the present invention have elevated levels cyclin E protein in the lung and have in increased occurrence of lung carcinogenesis. The animals of the instant invention were also found to have increased levels of Gli1 and Shh. Vectors, cells and cell lines are provided, as is a method for identifying a therapeutic agent for the chemoprevention or treatment of lung cancer.12-18-2008
20080313749Binding Compounds, Immunogenic Compounds and Peptidomimetics - The invention provides means and methods for producing compounds suitable for testing for the presence and/or identification of an immunogenic compound and/or a binding compound of interest. Immunogenic compounds and compositions are also herewith provided, as well as peptidomimetics of members of the cystine-knot family.12-18-2008
20090083864White hair development model animal, method for establishing white hair development model animal, method for passage of white hair development model animal, method for study on white hair development-control means, and composition for control of white hair development - A model animal causing the white hair development as a non-human mammalian animal with a phenotype such that the color of the hair first growing after birth is black or almost black and the model animal then causes the spontaneous white hair development following aging, where (1) the activated RET gene is genetically inserted in a hetero form and (2) the endothelin receptor B (Ednrb) gene is deficient in a hetero form, or the Ednrb gene is deficient in the homo form or in a hetero form and the Ednrb gene is genetically inserted in the homo form or in a hetero form under the DbH promoter.03-26-2009
20110055936TRANSGENIC MAMALS MODIFIELD IN BRI PROTEIN EXPRESSION - Provided are non-human mammals comprising a transgenic nucleic acid sequence capable of causing an alteration of expression of Bri2 or Bri3 in the mammal. Also provided are non-human mammals comprising a Bri2 or Bri3 gene under the control of the native Bri2 or Bri3 promoter. Additionally provided are non-human mammals genetically engineered to lack expression of a Bri2 or Bri3 gene. Further, non-human mammals comprising a transgene encoding a Bri2 or Bri3 protein under the control of the αCaMKII promoter are provided. Non-human mammals comprising a transgene encoding a furin protein are additionally provided. Embryonic stem cells of any of the above-described non-human mammals are further provided. Methods of screening a compound for treatment of a disease characterized by cerebral amyloidosis are additionally provided. Also provided are methods of making transgenic non-human mammals. Nucleic acids capable of causing an alteration of expression of Bri2 or BH3 if transfected into a mouse are additionally provided, as are comprising a sequence capable of causing an alteration of expression of Bri2 or Bri3 if transfected into a mouse.03-03-2011
20110055937Keratin 8 Mutations are Risk Factors for Developing Liver Disease of Multiple Etiologies - Keratin 8 and 18 (K8/K18) mutations are shown to be associated with a predisposition to liver or biliary tract disease, particularly noncryptogenic hepatobiliary disease. Unique K8/K18 mutations are shown in patients with diseases including but without limitation to viral hepatitis, biliary atresia, alcoholic cirrhosis and other acute or chronic toxic liver injury, cryptogenic cirrhosis, acute fulminant hepatitis, autoimmune liver disease, cystic fibrosis, primary biliary cirrhosis, primary sclerosing cholangitis, diseases that are linked with cryptogenic cirrhosis, such as nonalcoholic steatohepatitis, and the like. Livers with keratin mutations had increased incidence of cytoplasmic filamentous deposits. Therefore, K8/K18 are susceptibility genes for developing cryptogenic and noncryptogenic forms of liver disease. Mutant alleles are associated with disease susceptibility, and their detection is used in the diagnosis of a predisposition to these conditions.03-03-2011
20120151609Genetically Modified Rat Models for Pain - This invention relates to the engineering of animal cells, preferably mammalian, more preferably rat, that are deficient due to the disruption of gene(s) or gene product(s) resulting in altered nervous system function. In one aspect, the altered function results in pain in the mammal. In another aspect, the nervous system dysfunction results in prolonged hyperalgesia, allo dynia, and loss of sensory function. In another aspect, the invention relates to genetically modified rats, as well as the descendants and ancestors of such animals, which are animal models of altered nervous system function mediated pain and methods of their use. In another aspect, the genetically modified rats, as well as the descendants and ancestors of such animals, are animal models of nervous system dysfunction resulting in prolonged hyperalgesia, allodynia, and loss of sensory function and methods of their use. In another aspect, the present invention provides a method of identifying a compound useful for the treatment or prevention of pain.06-14-2012
20100275276ZEBRAFISH MODEL FOR ASSESSING GASTROINTESTINAL MOTILITY - The present invention has demonstrated the presence of the zebrafish KIT protein resulting from the expression of the kit gene in the zebrafish GI tract. As expression of the KIT protein is correlated with ICC in other species, the expression of the KIT protein in zebrafish indicates the presence of ICC in the zebrafish GI tract. ICC are required for spontaneous, coordinated contractions of GI smooth muscle. The present invention provides a zebrafish-based model system useful for elucidating the cellular and molecular mechanisms of gastrointestinal (GI) function and for identifying molecular targets for treating GI motility disorders in human.10-28-2010
20110016542CANINE GENOME EDITING WITH ZINC FINGER NUCLEASES - The present invention provides a genetically modified canine or cell comprising at least one edited chromosomal sequence. In particular, the chromosomal sequence is edited using a zinc finger nuclease-mediated editing process. The disclosure also provides zinc finger nucleases that target specific chromosomal sequences in the canine genome.01-20-2011
20110016539GENOME EDITING OF NEUROTRANSMISSION-RELATED GENES IN ANIMALS - The present invention provides genetically modified animals and cells comprising edited chromosomal sequences encoding proteins that are associated with neurotransmission disorders. In particular, the animals or cells are generated using a zinc finger nuclease-mediated editing process. Also provided are methods of using the genetically modified animals or cells disclosed herein to screen agents for toxicity and other effects.01-20-2011
20110016538Susceptibility locus for schizophrenia - Provided are methods for determining the susceptibility of an individual to a neuropsychiatric disorder, or a method of diagnosis or prognosis of the neuropsychiatric disorder (particularly schizophrenia) the methods comprising use of a pericentriolar material 1 (PCM1) marker which is located in the chromosomal region 8p21-22, for example a marker within the PCM1 gene locus or within 1000 kb of it. The invention also provides novel markers, and related materials and methods of detecting them, and identifying further molecules for use in therapy and diagnosis.01-20-2011
20110016541GENOME EDITING OF SENSORY-RELATED GENES IN ANIMALS - The present invention provides genetically modified animals and cells comprising edited chromosomal sequences encoding proteins that are associated with nociception or taste disorders. In particular, the animals or cells are generated using a zinc finger nuclease-mediated editing process. Also provided are methods of using the genetically modified animals or cells disclosed herein to screen agents for toxicity and other effects.01-20-2011
20110016540GENOME EDITING OF GENES ASSOCIATED WITH TRINUCLEOTIDE REPEAT EXPANSION DISORDERS IN ANIMALS - The present invention provides genetically modified animals and cells comprising edited chromosomal sequences encoding proteins that are associated with trinucleotide repeat expansion disorders. In particular, the animals or cells are generated using a zinc finger nuclease-mediated editing process. Also provided are methods of using the genetically modified animals or cells disclosed herein to screen agents for toxicity and other effects.01-20-2011
20110035814COOPERATING ONCOGENES IN CANCER - This invention provides methods of diagnosis, drug screening, and treatment based on the discovery that cIAP1 and Yap are co-amplified oncogenes that cooperate to contribute to oncogenesis and tumor maintenance.02-10-2011
20110072524Transgenic Mouse Lacking Endogenous FVIII and VWF - A Model of Hemophilia A - The present invention relates, generally, to a transgenic non-human animal model of hemophilia A, wherein the transgenic animal is deficient in endogenous Factor VIII and endogenous von Willebrand Factor, and methods to treat hereditary or acquired hemophilia A or von Willebrand Disease (VWD) by administration of exogenous human VWF.03-24-2011
20100325742Animal Model Based on Targeted Apoptosis for the Study of Genetic Diseases Such as Parkinson's Disease - Described is the use of a non-human transgenic animal, preferably a mouse, characterized in that it contains a modified version of the gene encoding TIF-IA (a) as an animal model for a disease, (b) for analyzing the function of selected stem cells or (c) for ablating malignant cells or microglia cells. Furthermore, methods for screening a therapeutic compound are described which comprise administering a candidate compound to said non-human transgenic animal (or a cell line derived from said non-human transgenic animal) and monitoring a therapeutic effect of said compound.12-23-2010
20110138488DEFICIENCY IN THE HISTONE DEMETHYLASE JHDM2A RESULTS IN IMPAIRED ENERGY EXPENDITURE AND OBESITY - The present invention relates to animal models of metabolic disorders such as obesity, diabetes, metabolic syndrome, insulin resistance, hyperinsulinemia, glucose intolerance, hyperlipidemia, and the like. In particular, the invention relates to transgenic non-human animals having a reduction in functional Jhdm2a gene expression and use of such animals and cells having reduced Jhdm2a expression in drug discovery. The invention further relates to the identification of subjects having or at increased risk for developing a metabolic disorder based on a genetic marker in the Jhdm2a gene.06-09-2011
20090210950METHODS FOR SCREENING FOR AGENTS THAT AFFECT DEVELOPMENT - The present invention provides an animal toxicity model that can be used to screen agents that may cause or increase the occurrence of a developmental defect. The invention also provides methods and compositions for creating such an animal toxicity model, as well as methods and kits for using these animal models.08-20-2009
20090210949METHOD OF AMELIORATING SYMPTOM CAUSED BY MOOD DISTURBANCE - The present invention relates to a method for improving symptom of mood disorder or its related disorder comprising a step of allowing Gm1 protein and the like to be excessively present in a brain of a mammal, and a non-human mammal, to which the method has been applied, and the like.08-20-2009
20110016537Cellular model of tauopathies for lead identification and drug discovery - The present invention provides polypeptides with modified microtubule binding domains of a tau protein, which polypeptides lead to an increase of neurofibrillary tangles when introduced into a cell. The invention further provides nucleic acid molecules encoding these polypeptides, cells comprising the polypeptides and transgenic animals with cells expressing these polypeptides. The polypeptides of the invention form the basis for animal and cellular models of tau pathology, which form the basis for molecular screens for biomolecules involved in tauopathies, but also for medicaments useful for the treatment of tauopathies.01-20-2011
20110072525COMPOSITIONS AND METHODS FOR THE TREATMENT OF PSYCHIATRIC AND NEUROLOGICAL DISORDERS - The present invention relates to mutant animals having a modified NMDA Receptor and use of the same for screening compounds useful for treating psychiatric and neurological disorders, such as schizophrenia, autism and Alzheimer's Disease. In particular, the invention provides an animal model that has mutation in phosphorylation of the NR1 subunit of the NMDAR, which causes behavioral deficits associated with psychiatric disorders useful for the evaluation of the therapeutic effects of psychotropic drugs for the treatment of these disorders.03-24-2011
20100077492Oxidative DNA Damage Protection - Provided herein are methods of screening compounds, gene sequences, and gene products in bacteria for agents that are protective against oxidative DNA damage in a human or animal. Gene sequences identified by these screens can also be used in diagnostic assays that identify subjects at increased risk for oxidative DNA damage. Pharmaceutical compositions that include DNA protective agents identified by these screens are also provided.03-25-2010
20100077491Modulators of RNF5 and Uses Thereof - Provided herein are compositions and methods relating to the involvement of RNF5 in muscle wasting.03-25-2010
20100077490Animal model exhibiting cancer, pulmonary emphysema and cardiomyopathy - A transgenic mouse model for colorectal cancer, pulmonary emphysema or cardiomyopathy comprises a transgenic mouse that produces suboptimal levels of latent transforming growth factor β binding protein 4 (LTBP-4). The transgenic mouse includes a mutation resulting in homozygous disruption of both endogenous alleles of a gene encoding LTBP-4, and develops colorectal cancer, pulmonary emphysema or cardiomyopathy.03-25-2010
20100235927NON-HUMAN ANIMAL MODEL FOR LUNG CARCINOMA - A transgenic mouse expressing JSRV Env transgene that is operably linked to a surfactant protein C promoter (SPCp) is disclosed. The transgenic mouse is prone to developing a lung tumor and serves as an animal model for human lung carcinoma.09-16-2010
20090293137Novel Gene Disruptions, Compositions and Methods Relating Thereto - The present invention relates to transgenic animals, as well as compositions and methods relating to the characterization of gene function. Specifically, the present invention provides transgenic mice comprising disruptions in PRO218, PRO228, PRO271, PRO273, PRO295, PRO302, PRO305, PRO326, PRO386, PRO655, PRO162, PRO788, PRO792, PRO940, PRO941, PRO1004, PRO1012, PRO 1016, PRO474, PRO5238, PRO1069, PRO1111, PRO1113, PRO1130, PRO1195, PRO1271, PRO1865, PRO1879, PRO3446, PRO3543, PRO4329, PRO4352, PRO5733, PRO9859, PRO9864, PRO9904, PRO9907, PRO10013, PRO90948, PRO28694, PRO16089, PRO19563, PRO19675, PRO20084, PRO21434, PRO50332, PRO38465 or PRO346 genes. Such in vivo studies and characterizations may provide valuable identification and discovery of therapeutics and/or treatments useful in the prevention, amelioration or correction of diseases or dysfunctions associated with gene disruptions such as neurological disorders; cardiovascular, endothelial or angiogenic disorders; eye abnormalities; immunological disorders; oncological disorders; bone metabolic abnormalities or disorders; lipid metabolic disorders; or developmental abnormalities.11-26-2009
20110265192NUCLEAR RECEPTOR SENSOR SYSTEM IN TRANSGENIC ANIMAL - A sensor system for detecting the activation of specific nuclear receptors in a tissue of an animal is provided. The nuclear receptor sensor system comprises a sensor component comprising a nuclear receptor or part thereof coupled to a DNA-binding domain, and a reporter component comprising a reporter gene. Transgenic animals, such as a transgenic pig is provided, which comprises the components of the nuclear receptor sensor system in its genome. Also methods of producing the transgenic animal is provided as well as use of the transgenic animal for evaluating the activity of a nuclear receptor in vivo.10-27-2011
20100031379NON-HUMAN ANIMAL FOR EYE DISEASE MODEL - It is intended to provide an animal model which shows a naturally occurring eye disease symptom, particularly ocular hypertension and/or retinal degeneration. The invention relates to a non-human animal for eye disease model in which the function of Vav2 gene and/or Vav3 gene have/has been impaired. Because the animal shows a naturally occurring eye disease symptom, such as ocular hypertension and/or retinal degeneration without administering a drug or placing it in a special growth environment, it can be used as a model useful for elucidation of onset mechanism of eye disease or evaluation for therapeutic agent for eye disease. When it is applied for such a purpose, because it is not affected by an exogenous factor, which is conventionally administered for artificially inducing eye disease, it reflects a natural pathology, therefore, the clinical and industrial usefulness thereof is high.02-04-2010
20100031378Novel gene disruptions, compositions and methods relating thereto - The present invention relates to transgenic animals, as well as compositions and methods relating to the characterization of gene function. Specifically, the present invention provides transgenic mice comprising disruptions in PRO227, PRO233, PRO238, PRO1328, PRO4342, PRO7423, PRO10096, PRO21384, PRO353 or PRO1885 genes. Such in vivo studies and characterizations may provide valuable identification and discovery of therapeutics and/or treatments useful in the prevention, amelioration or correction of diseases or dysfunctions associated with gene disruptions such as neurological disorders; cardiovascular, endothelial or angiogenic disorders; eye abnormalities; immunological disorders; oncological disorders; bone metabolic abnormalities or disorders; lipid metabolic disorders; or developmental abnormalities.02-04-2010
20100031377Prevention and treatment of synucleinopathic and amyloidogenic disease - The invention provides improved agents and methods for treatment of diseases associated with synucleinopathic diseases, including Lewy bodies of alpha-synuclein in the brain of a patient. Such methods entail administering agents that induce a beneficial immunogenic response against the Lewy body. The methods are particularly useful for prophylactic and therapeutic treatment of Parkinson's disease.02-04-2010
20100024047Prion-free transgenic ungulates - Transgenic and cloned ungulates and particularly cloned cattle are disclosed, wherein such cattle contain a deletion or disruption of the prion gene locus and do not express functional prion protein, and are not susceptible to prion-related diseases such as bovine spongiform encephalopy or Mad Cow Disease.01-28-2010
20100017898THERAPEUTIC APPLICATIONS OF NONCOVALENT DIMERIZING ANTIBODIES - Compositions and methods for providing antibodies having noncovalent, self-binding properties are disclosed. Such autophilic antibodies can bind cellular receptors to promote apoptosis of target cells and enhance therapeutic efficacies in the treatment of patients with debilitating or life-threatening diseases. Representative diseases targeted by the autophilic antibodies are lymphomas, breast cancers, colon cancers, and melanomas. Autoimmune disorders, Alzheimer's disease, and other neuro-degenerative conditions, as well as graft or transplant rejection, are among other treatable conditions.01-21-2010
20100017896Filaggrin - The present invention relates to the identification of loss-of-function mutations in the filaggrin gene and their use in diagnosing ichthyosis vulgaris and/or susceptibility to other diseases including atopic dermatitis (eczema), asthma, psoriasis and allergies (including food allergy).01-21-2010
20100017895Small animal model for hcv replication - An animal model for HCV replication and/or production of virus or virus like particles is provided. The invention utilizes an HCV replicon present in a cell to deliver HCV nucleic acid and replicate and express HCV proteins in an animal model comprising an animal that has been immunocompromised. The invention further provides a method of treatment or prevention of HCV in a mammal which comprises administering to the mammal a combination which comprises an immunomodulatory compound and another antiviral agent. Also provided are cell lines showing a decreased sensitivity to interferon alpha or some other immunomodulator and methods of making or isolating such cell lines.01-21-2010
20090077676PREMATURELY AGEING MOUSE MODELS FOR THE ROLE OF DNA DAMAGE IN AGEING AND INTERVENTION IN AGEING-RELATED PATHOLOGY - The current invention pertains to a method for screening and discovery of compounds capable of inhibiting, preventing, delaying or reducing genome maintenance disorders and consequences thereof, in particular ageing related symptoms and disorders. The current invention provides a method for screening and discovery of compounds that are capable of inhibiting, preventing, delaying or reducing genome maintenance disorders and consequences thereof. The invention exploits animal models that comprise deficiencies in their genome maintenance systems, such as DNA repair systems, and display premature, enhanced, accelerated or segmental ageing phenotypes. These animal models can be advantageously applied to screen compounds and thereby develop schemes of intervention to treat, delay, inhibit, prevent or cure ageing related symptoms. The current invention thus provides a new and powerful tool to screen aid/or discover therapeutically active compounds to treat ageing related symptoms and diseases. On the same basis it permits screening and discovery of compounds that influence ischemia, reperfusion damage in organ/tissue transplantation, chemotherapy and stem cell transplantation.03-19-2009
20090100532TRANSGENIC MICE EXPRESSING HYPERSENSITIVE NICOTINIC RECEPTORS - Provided herein are transgenic non-human animals having a transgene encoding a variant nicotinic acetylcholine receptor (nAChR) subunit, wherein the variant nAChR subunit is selected from the group consisting of α6, α5, and β2. The transgenic animals display a modified phenotype that includes nicotinic hypersensitivity. Also provided are methods of generating the invention transgenic animals. Further provided are methods for screening a candidate agent for the ability to modulate nicotine-mediated behavior in the invention transgenic animals.04-16-2009
20090113561GENE TRAP CASSETTES FOR RANDOM AND TARGETED CONDITIONAL GENE INACTIVATION - A new type of gene trap cassette, which can induce conditional mutations, relies on directional site-specific recombination systems, which can repair and re-induce gene trap mutations when activated in succession. After the gene trap cassettes are inserted into the genome of the target organism, mutations can be activated at a particular time and place in somatic cells. The gene trap cassettes also create multipurpose alleles amendable to a wide range of post-insertional modifications. Such gene trap cassettes can be used to mutationally inactivate all cellular genes temporally and/or spatially. Cells which contain the inventive gene trap cassette can be used for identification and/or isolation of genes and for the creation of transgenic organisms to study gene function at various developmental stages, including the adult, as well as for the creation of animal models of human disease useful for in vivo drug target validation.04-30-2009
20110154513PROBE FOR VISUALIZING NEURAL ACTIVITY - An object of the present invention is to develop a probe for measuring in real time the kinetics of CREB or actin closely related to brain functions such as memory formation in live animals. The probe used in the present invention is a probe comprising luciferase split into N-terminal and C-terminal fragments, wherein the probe is selected from any one or more of: (1) a probe comprising the KID domain of cyclic AMP response element-binding protein (CREB), the KIX domain of CREB-binding protein (CBP), the N-terminal fragment of luciferase (LucN), and the C-terminal fragment of luciferase (LucC) in one molecule; (2) (a) a probe consisting of two molecules, one of which comprises LucN and the KID domain and the other of which comprises LucC and the KIX domain, or (b) a probe consisting of two molecules, one of which comprises LucN and the KIX domain and the other of which comprises LucC and the KID domain; and (3) a probe consisting of two molecules, one of which comprises actin and LucN and the other of which comprises actin and LucC.06-23-2011
20090172827Kcnn3 as diagnostic and therapeutic target for neurodegenerative diseases - The present invention discloses a dysregulation of the KCNN3 gene and the protein products thereof in Alzheimer's disease patients and individuals being at risk of developing Alzheimer's disease. Based on this finding, the invention provides methods for diagnosing and prognosticating Alzheimer's disease in a subject, and for determining whether a subject is at increased risk of developing Alzheimer's disease. Furthermore, this invention provides therapeutic and prophylactic methods for treating and preventing Alzheimer's disease and related neurodegenerative disorders using the KCNN3 gene and its corresponding gene products. Screening methods for modulating agents of neurodegenerative diseases are also disclosed.07-02-2009
20120042398COMPOSITIONS FOR LABELING AND IDENTIFYING AUTOPHAGOSOMES AND METHODS FOR MAKING AND USING THEM - The invention provides methods and compositions for detecting and measuring the amount of autophagosomes in cells or tissues, including biopsy samples, in vitro, in situ and/or in vivo. By detecting and measuring the amount of autophagosomes in cells or tissues, the methods and compositions of the invention also measure the amount of autophagic activity in a cell or a tissue. In one aspect, the invention can be adapted to a plate-reader format for high-throughput screening of drugs that modulate autophagy, i.e., high-throughput detection of autophagic (autophagosome) activity in cells or tissues. In alternative embodiments, the compositions of the invention can localize into autophagosomes (AV), and these compositions can comprise any detectable moiety or group, e.g., a cadaverine, a radioactive, fluorescent-, bioluminescent and/or paramagnetic-conjugated reagent.02-16-2012
20090031433METHODS FOR SCREENING INSECTICIDES - The present invention relates to methods of screening for potential insecticidal agents using genes encoding proteins that regulate xenobiotic detoxification in insects. In particular the invention relates to methods of using insect nuclear hormone receptor genes, in particular dhr96 or homologues thereof and/or their promoters. Such methods employ inter alia transgenic cells and/or transgenic whole organisms in which one or more nuclear hormone receptor gene is deleted or under-expressed.01-29-2009
20120210449NOVEL TRANSPARENT ZEBRAFISH AND PREPARATION METHOD THEREOF - This invention provides a biological selective breeding technique in preparation of a transparent zebrafish, Citrine. The appearance of Citrine is transparent and yellowish, with uniformly pigmented black eyes and its inner organs are observable by eyes. The invention also provides a method for in vivo observation of progression and expansion of various disease stages or physiological processes.08-16-2012
20120210450Novel gene disruptions, compositions and methods relating thereto - The present invention relates to transgenic animals, as well as compositions and methods relating to the characterization of gene function. Specifically, the present invention provides transgenic mice comprising disruptions in PRO194, PRO220, PRO241, PRO284, PRO331, PRO354, PRO355, PRO533, PRO541, PRO725, PRO937, PRO1014, PRO1120, PRO1182, PRO1325, PRO1382, PRO1410, PRO1555, PRO1556, PRO1760, PRO1787, PRO1868, PRO4326, PRO4332, PRO4346, PRO4400, PRO6003, PRO6094, PRO6244, PRO9820, PRO9828, PRO10274, PRO16090, PRO19644, PRO21340, PRO92165, PRO85143, PRO1124, PRO1026 or PRO23370 genes. Such in vivo studies and characterizations may provide valuable identification and discovery of therapeutics and/or treatments useful in the prevention, amelioration or correction of diseases or dysfunctions associated with gene disruptions such as neurological disorders; cardiovascular, endothelial or angiogenic disorders; eye abnormalities; immunological disorders; oncological disorders; bone metabolic abnormalities or disorders; lipid metabolic disorders; or developmental abnormalities.08-16-2012
20090187996Ion Channel - The present invention relates to a method of identifying a molecule suitable for the treatment, prophylaxis or alleviation of pain, the method comprising determining whether a candidate molecule is an agonist or antagonist, including a opener, blocker or modulator, of Kv9.2 polypeptide, in which the Kv9.2 polypeptide comprises the amino acid sequence shown in SEQ ID NO:3 or SEQ ID NO:5, or a sequence which is at least 90% identical thereto.07-23-2009
20120005765ANIMAL MODEL FOR PARKINSON'S DISEASE - Disclosed are methods and compositions for an animal model of Parkinson's disease. In particular, disclosed is the use of antisense compounds to inhibit the expression of ALDH1A1 in the substantia nigra of an animal brain for the purpose of creating an animal that will displays the symptoms of a human with Parkinson's Disease, including various biochemical, histological, and behavioral characteristics. Also disclosed are methods for using the animal model for Parkinson's disease to test potential therapeutic agents for Parkinson's disease.01-05-2012
20120005766Methods of identifying agents that modulate phenotypes related to disruptions, of a gene encoding PRO235 polypeptide - The present invention relates to transgenic animals, as well as compositions and methods relating to the characterization of gene function. Specifically, the present invention provides transgenic mice comprising disruptions in PRO188, PRO235, PRO266, PRO337, PRO361, PRO539, PRO698, PRO717, PRO846, PRO874, PRO98346, PRO1082, PRO1097, PRO1192, PRO1268, PRO1278, PRO1303, PRO1308, PRO1338, PRO1378, PRO1415, PRO1867, PRO1890, PRO3438, PRO19835, PRO36915, PRO36029, PRO4999, PRO5778, PRO5997, PRO6079, PRO6090, PRO7178, PRO21184, PRO7434, PRO9822, PRO9833, PRO9836, PRO9854, PRO9862, PRO10284, PRO37510, PRO35444, PRO20473, PRO21054 or PRO35246 genes. Such in vivo studies and characterizations may provide valuable identification and discovery of therapeutics and/or treatments useful in the prevention, amelioration or correction of diseases or dysfunctions associated with gene disruptions such as neurological disorders; cardiovascular, endothelial or angiogenic disorders; cyc abnormalities; immunological disorders; oncological disorders; bone metabolic abnormalities or disorders; lipid metabolic disorders; or developmental abnormalities.01-05-2012
20110167506METHOD FOR EVALUATION OF DEVELOPMENTAL TOXICITY - The present invention provides a method for assessing embryotoxicity of a chemical comprising: (1) a first step of measuring the expression level of one or more genes selected from among genes each comprising any of the nucleotide sequences of SEQ ID NOs: 1 to 78 and 101 to 230 and orthologous genes thereof in a sample from a non-human mammal or mammalian cell which has come into contact with a test chemical; and (2) a second step of comparing the measured value of the expression level of the gene in the sample obtained in the first step with a control value of the expression level of the gene and based on the difference assessing the level of the embryotoxicity of the test chemical in the sample; and so on.07-07-2011
20110167505GFATS As Modifiers of the AXIN Pathway and Methods of Use - Human GFAT genes are identified as modulators of the Axin pathway, and thus are therapeutic targets for disorders associated with defective Axin function. Methods for identifying modulators of Axin, comprising screening for agents that modulate the activity of GFAT are provided.07-07-2011
20080313747Targeted Transgenesis of Short Hairpin Rna Expression Cassettes Using Recombinase Mediated Cassette Exchange - The invention provides a method for targeted transgenesis of short hairpin RNA expression cassettes using recombinase mediated cassette exchange. Suitable nucleotide acid sequences and vectors for the targeted transgenesis and recombinase mediated transgenesis are provided.12-18-2008
20120117668NUCLEIC ACID EXPRESSION CONSTRUCT AND ITS USE AS A CELL PROLIFERATION MARKER - A nucleic acid expression construct which encodes a fusion protein includes a reporter protein and a protein with a wild-type destruction signal. A sequence encoding the fusion protein is operably linked to a non-endogenous promoter. The fusion protein localizes during a cell cycle progression to subcellular structures selected from a cell cortex, a contractile ring, and a midbody.05-10-2012
20120180141Transgenic Animal Models of Disease - The present invention provides transgenic, large non-human animal models of diseases and conditions, as well as methods of making and using such animal models in the identification and characterization of therapies for the diseases and conditions.07-12-2012
20120023599GENOME EDITING OF CYTOCHROME P450 IN ANIMALS - The present invention provides genetically modified animals and cells comprising edited chromosomal sequences encoding cytochrome P450 (CYP) proteins. In particular, the animals or cells are generated using a zinc finger nuclease-mediated editing process. The invention also provides zinc finger nucleases that target chromosomal sequence encoding CYP proteins, as well as methods of using the genetically modified animals or cells disclosed herein to screen agents for toxicity and other effects.01-26-2012
20120159653GENOMIC EDITING OF GENES INVOLVED IN MACULAR DEGENERATION - The present invention provides genetically modified animals and cells comprising edited chromosomal sequences encoding proteins associated with MD. In particular, the animals or cells are generated using a zinc finger nuclease-mediated editing process. Also provided are methods of using the genetically modified animals or cells disclosed herein to study MD development and methods of assessing the effects of agents in genetically modified animals and cells comprising edited chromosomal sequences encoding proteins associated with MD.06-21-2012
20120159656COMPOSITIONS AND METHODS FOR EVALUATING COGNITIVE DEFECTS - The present invention provides, in some aspects, methods for identifying agents useful in treating disorders or conditions associated with cognitive deficits. In some aspects, the invention provides methods for detecting a cognitive deficit in a subject.06-21-2012
20120159655METHODS USING AXL AS A BIOMARKER OF EPITHELIAL-TO-MESENCHYMAL TRANSITION - The present invention relates to the use of AxI as a biomarker for detecting the occurrence of epithelial-to-mesenchymal transition (EMT) in a subject. More specifically, the invention relates to various methods for detecting the occurrence of epithelial-to-mesenchymal transition (EMT) in a subject by measuring AxI expression and/or activity.06-21-2012
20120159654GENOME EDITING OF GENES INVOLVED IN ADME AND TOXICOLOGY IN ANIMALS - The present invention provides genetically modified animals and cells comprising edited chromosomal sequences involved in ADME and toxicology. In particular, the animals or cells are generated using a zinc finger nuclease-mediated editing process. The invention also provides zinc finger nucleases that target chromosomal sequence involved in ADME and toxicology and the nucleic acids encoding said zinc finger nucleases. Also provided are methods of assessing the effects of agents in genetically modified animals and cells comprising edited chromosomal sequences involved in ADME and toxicology.06-21-2012
20080313751Method by Using Human or Mice-Isg12 to Develop and Prepare Drugs and Single Nucleotide Polymorphism in the Isg12 Gene for Diagnostic Use - Here is described a novel gene, the interferon inducible gene 12 (ISG12, IFI27), that interacts with nuclear receptors and enhances nuclear export of such transcription factors. As a consequence, the transcriptional activities of these nuclear receptors are decreased. As examples effects on NR4A1 and PPARa and PPARg are given. When ISG12 is absent as in ISG12 deficient mice transcriptional activities of these nuclear receptors are not impaired and their protective effects are fully appreciated. Consistently, ISG12 deficient mice are resistant to restenosis upon carotid artery ligation and to endotoxin induced death. Human genetics studies indicate the importance of ISG12 where the inventors could show a strong association between an intronic ISG12 SNP and the presence of hypercholesterolemia, diabetes type 2 and stroke. ISG12 is therefore a target for novel therapeutic strategies for the treatment of vascular diseases.12-18-2008
20100115636PIG MODEL FOR BREAST CANCER, MITOCHONDRIA RELATED PROTEIN FOLDING DISORDERS AND/OR EPIDERMOLYSIS BULLOSA SIMPLEX - The present invention relates to a genetically modified pig as a model for studying breast cancer, mitochondria related protein folding disorders and/or epidermolysis bullosa simplex. The modified pig model displays one or more phenotypes associated with any of said disorders. Disclosed is also a modified pig comprising a modified endogeneous BRCA1 and/or BRCA 2 gene, and/or a modified ornithine transcarbamylase gene, and/or a modified Keratin 14 gene and/or a transcriptional or translational product or part thereof. The invention further relates to methods for producing the modified pig; and methods for evaluating the effect of a therapeutical treatment of breast cancer, mitochondria related protein folding disorders and/or epidermolysis bullosa simplex; methods for screening the efficacy of a pharmaceutical composition; and a method for treatment of a human being suffering from breast cancer, mitochondria related protein folding disorders and/or epidermolysis bullosa simplex are disclosed.05-06-2010
20110107440SKIN CANCER ASSOCIATED MICRORNAS - This invention relates to the finding that skin cancers, such as squamous cell carcinoma and basal cell carcinoma, are characterized by changes in the expression of specific microRNA molecules (miRNAs). These miRNAs may therefore be useful as biomarkers for skin cancers as well as therapeutic targets. Methods of diagnosis and treatment of skin cancers are provided, as well as methods of screening for therapeutic compounds.05-05-2011
20110099644MIG-6 KNOCKOUT MICE AND ELUCIDATION OF ASSOCIATION OF MIG-6 WITH EARLY ONSET DEGENERATIVE JOINT DISEASE AND ROLE AS A TUMOR SUPPRESSOR - The molecular mechanism underlying degenerative joint disease, also known as osteoarthritis (OA), is not fully understood. Disruption of mitogen inducible gene 6 (Mig-6) in mice by homologous recombination (KO mice) led to early onset OA as revealed by simultaneous enlargement and deformity of multiple joints, degradation of articular cartilage and the development of bony outgrowths or osteophytes within the joint space. The latter appeared to be derived from proliferation of mesenchymal progenitor cells followed by differentiation into chondrocytes. Because of the striking similarity to human OA, Mig-6 KO mice are a useful animal model for studying the mechanism of this disease and for testing new drugs or therapies for treating OA. These KO mice also developed epithelial hyperplasia, adenoma, and adenocarcinoma in organs such as lung, gallbladder, and bile duct. Mig-6 is therefore a tumor suppressor gene and is a candidate gene for the frequent Ip36 genetic alterations found in lung cancer. It can be used as a tumor biomarker as well as a target for cancer therapy. Mig-6 is located in human chromosome Ip36, a locus frequently associated with human lung cancer. Mig-6 is a negative regulator of EGF signaling, and like EGF, was induced by HGF/SF in human lung cancer cell lines. Frequently the receptors EGFR and Met were co-expressed, and Mig-6 was induced by both EGF and HGF/SF in a MAPK-dependent fashion. Not all tumor lines express Mig-6 in response to either EGF or HGF/SF. In these cases, missense and nonsense mutations in the Mig-6 coding region were found, as was evidence for Mig-6 transcriptional silencing.04-28-2011
20090133133Transgenic Mice for Bioassay of Prions from Deer and Elk with Chronic Wasting Disease - The invention relates to the use of transgenic constructs to produce animal models for the study of chronic wasting disease.05-21-2009
20120233713METHODS AND SYSTEMS FOR INDUCIBLE ABLATION OF NEURAL CELLS - The present invention relates to methods and systems for inducible ablation of neural cells, in particular non-proliferating cells, such as oligodendrocytes and Schwann cells. The methods and systems include an animal model that can be specifically induced to display phenotypic traits or characteristics of a demyelination condition. The methods and systems disclosed herein are useful for drug screening, by identifying compounds or agents that promote remyelination or reversal of phenotypic traits or characteristics of demyelination conditions.09-13-2012
20120222139Cancer Specific Mitotic Network - Developed here is a mitotic network comprising a signature of up to 54 genes, and including also sub-sets of genes within the signature, which can identify members by requiring higher correlation values for a signature gene. The present mitotic network provides for methods for prognosis and diagnosis of various cancers. The mitotic network is conserved across cancers exhibiting aberrant mitotic activity and several genes in the network act as therapeutic targets. Development of other inhibitors of mitosis can apply expression values of the genes in the mitotic network from patient tissue to select patients during clinical validation of the new drugs.08-30-2012
20120131687AGENT THAT MODULATES PHYSIOLOGICAL CONDITION OF PESTS, INVOLVED IN INSECT VOLTAGE-GATED POTASSIUM CHANNEL ACTIVITY - The present invention provides an agent that modulates physiological condition of pests, wherein the agent has an ability to modulate the activity of an insect voltage-gated potassium channel; a method for assaying pesticidal activity of a test substance, which comprises measuring the activity of a voltage-gated potassium channel in a reaction system in which the voltage-gated potassium channel contacts with a test substance, and so on.05-24-2012
20120167236METHOD OF PREDICTING A BEHAVIOR OF ONE OR MORE DRUGS - The present invention is directed to the production, breeding and use of transgenic non-human animals such as mice in which specific genes or portions of genes have been replaced by homologues from another animal to make the physiology of the animals so modified more like that of the other animal with respect to drug pharmacokinetics and metabolism. The invention also extends to the use of the genetically modified non-human animals of the invention for pharmacological and/or toxicological studies.06-28-2012
20120216302METHODS AND ASSAYS FOR TREATING SUBJECTS WITH SHANK3 DELETION, MUTATION OR REDUCED EXPRESSION - Methods and assays are disclosed for treating subjects with 22q13 deletion syndrome or SHANK3 deletion or duplication, mutation or reduced expression, where the methods comprise administering to the subject insulin-like growth factor 1 (IGF-1), IGF-1-derived peptide or analog, growth hormone, an AMPAkine, a compound that directly or indirectly enhances glutamate neurotransmission, including by inhibiting inhibitory (most typically GABA) transmission, or an agent that activates the growth hormone receptor or the insulin-like growth factor 1 (IGF-1) receptor, or a downstream signaling pathway thereof08-23-2012
20120137378EXTRANEOUS AGENTS TESTING - The present invention belongs to the field of pharmaceutical industry and specifies a method for testing extraneous agents in a composition comprising at least one active agent, comprising the steps of: a) contacting an antibody, which had been raised against an expression product of a polynucleotide construct comprising a sequence encoding at least a part of the active agent, with the composition comprising at least one active agent, wherein the antibody binds to the active agent, and b) determining the presence or absence of extraneous agents in the composition subsequent to step a). Furthermore, the invention specifies a process for producing a pharmaceutical composition by carrying out said method, to the use of a polynucleotide construct for testing the presence or absence of the active agent or of any extraneous or infectious agent in a composition to be tested. The present invention also relates to particular polynucleotides and polynucleotide constructs as useful substances in the field of influenza vaccines, as well as non-human organisms, transgenic animals or microorganisms containing the polynucleotides and/or polynucleotide constructs. The present invention is also directed to kit of parts.05-31-2012
20100175139SOMATOTRANSGENIC BIOIMAGING - The invention relates to modelling diseases, to screening for compounds that modulate such diseases and to as-saying drug metabolism and toxicity in non-human transgenic animals, by a novel technique developed by the inventors known as “somatotransgenic bioimaging”. The invention thus provides: a method for determining whether the expression of a reporter gene is modulated by a compound or a method of evaluating the metabolism and/or toxicity of a compound, said method comprising: (a) administering said compound to a non-human transgenic animal, generated by gene transduction of one or more specific tissues when in utero or neonatal, with a vector comprising a bioluminescent reporter gene operably linked to a genetic element responsive to a pathology or therapy or to a genetic element responsive to drug metabolism and/toxicity; and (b) determining whether or not of said compound has an effect on the expression of said reporter gene in said specific tissue or tissues and/or determining the extent of any such effect, said determination comprising detecting from the animal bioluminescence caused by the activity of the gene product of the reporter gene. In some embodiments cells pre-transduced with vectors of the invention may also be introduced into the animals instead of delivering the vectors directly.07-08-2010
20120255040Cell Model and Methods Using the Same - The present invention relates in a first aspect to a cell model containing chondrocytes whereby said chondrocytes contain a first heterologous nucleic acid sequence operably linked with a mb1 promoter sequence. In another aspect, the present invention relates to a cell model, in particular, to a transgenic animal model whose genome comprises a first heterologous nucleic acid sequence encoding a recombinase and/or restriction enzyme operably linked to a chondrocyte specific promoter, and a second heterologous nucleic acid sequence encoding a target peptide of interest wherein the second nucleic acid sequence further comprises recombination sequences or restriction site for the enzyme encoded by the first heterologous nucleic acid sequence. In addition, methods for screening foreign agent or methods for testing the efficacy and/or efficiency of an agent are provided. Said agents are tested for their ability to reduce or prevent or to allow treatment of diseases, disorders or conditions involving arthropathy and/or chondropathy, in particular, spinal malfunction.10-04-2012
20120317663METHODS OF SCREENING AGENTS FOR ACTIVITY USING TELEOSTS - The present invention provides methods of screening an agent for activity using teleosts. Methods of screening an agent for angiogenesis activity, toxic activity and an effect cell death activity in teleosts are provided. Methods of screening an agent for an activity in the brain or central nervous system in zebrafish are provided. The invention further provides high throughput methods of screening agents in multi-well plates.12-13-2012
20120174239Novel PRO1199 gene disruptions, and methods relating thereto - The present invention relates to transgenic animals, as well as compositions and methods relating to the characterization of gene function. Specifically, the present invention provides transgenic mice comprising disruptions in PRO224, PRO9783, PRO1108, PRO34000, PRO240, PRO943, hu A33, PRO230, PRO178, PRO1199, PRO4333, PRO1336, PRO19598, PRO1083, hu TRPM2 or PRO1801 genes.07-05-2012
20100299765MODALITIES FOR THE TREATMENT OF DEGENERATIVE DISEASES OF THE RETINA - This invention relates to methods for improved cell-based therapies for retinal degeneration and for differentiating human embryonic stem cells and human embryo-derived into retinal pigment epithelium (RPE) cells and other retinal progenitor cells.11-25-2010
20100050276Transgenic non-human animal models of apoptosis-mediated conditions - A transgenic non-human animal whose genome comprises a stable integration of a transgene that encodes at least one Fas-ligand protein operably-linked to a tetracycline-inducible promoter includes cells that express the transgene and undergo apoptosis. The transgenic non-human animal can be used to screen for compounds that inhibit apoptosis and to identify cells that are capable of differentiating in vivo.02-25-2010
20100050277KNOCKOUT ANIMAL EXHIBITING ANXIETY-LIKE BEHAVIOR - A vector for creating kf-1 gene knockout nonhuman animals exhibiting increased anxiety-like behaviors, and containing Lox-pM-M-kf-1[in3b]-kf-1[ex4a]-LoxP,02-25-2010
20100275274MOUSE MODEL FOR DEPRESSION, SCHIZOPHRENIA AND ALZHEIMER'S DISEASE - The present invention relates to Glycine N-methyltransferase (GNMT) animal model and use thereof.10-28-2010
20120180145Tool for Studying Endothelial Haematopoietic Transition (EHT) and Epithelial-Mesenchymal Transition (EMT) Associated Events - The present invention relates to the field of endothelial haematopoietic transition (EHT) and epithelial-mesenchymal transition (EMT) and more particularly relates to the use of fish embryo or larva as a model for the study of EHT and EMT.07-12-2012
20120180144ANIMAL MODELS OF NEUROLOGICAL DISORDERS - The present invention relates to the field of neurological disorders and more particularly to the field of neuropsychiatric disorders. The invention provides non-human, transgenic animal models for brain disorders such as schizophrenia, bipolar disorders, compulsive disorders, addictive disorders and the like. The animals also have applications in the field of GABA neuro-transmission and other disorders in which GABA-dependent gene regulation has a role.07-12-2012
20120180143TRANSGENIC ANIMAL MODEL OF NEURODEGENERATIVE DISORDERS - The present invention provides a transgenic animal model of Alzheimer's Disease designated TgCRND8 as well as a method for making such model, which allows for the characterization of the etiology of the disease as well as for provide a system for the development and testing of potential treatments.07-12-2012
20120180142CLONED TRANSMEMBRANE RECEPTOR FOR 24-HYDROXYLATED VITAMIN D COMPOUNDS AND USES THEREOF - The instant invention relates to the use of 24-hydroxylated vitamin D compounds as therapeutics in mammalian bone fracture repair. In addition, the instant invention relates to novel 24-hydroxylated vitamin D compound receptors which can be employed in the development of compounds capable of facilitating fracture repair in animals. The instant invention also relates to nucleic acids encoding such receptors as well as vectors, host cells, transgenic animals comprising such nucleic acids and screening assays employing such receptors.07-12-2012
20100011453MODEL FOR MUSCULAR DYSTROPHY AND CARDIOMYOPATHY - An isolated zebrafish genetic strain having a dystrophin mutant phenotype and fish models useful for screening or assaying agents having potential activity on muscular dystrophy or cardiomyopathy.01-14-2010
20100011451PHENOTYPIC AND GENOTYPIC DIFFERENCES OF MVA STRAINS - The present invention provides kits and methods to screen viral nucleic acids for a profile of genetic deletions and mutations, optionally in combination with one or more assays for viral replication and/or attenuation capacity.01-14-2010
20100011450IMMUNODEFICIENT MICE TRANSGENIC FOR HLA CLASS I AND HLA CLASS II MOLECULES AND THEIR USES - The invention relates to mice which are genetically deprived of T, B lymphocytes and NK cells, deficient for murine MHC class I and/or MHC class II molecules, and transgenic for the expression of the HLA class I and/or HLA class II molecules, and to their use as recipient hosts for the transplantation of human haematopoietic precursors, to study the human adaptative immune system development and function in vivo. The invention relates also to the applications of this human/mouse chimera model to improve immunotherapy against pathogens, cancer and autoimmune diseases.01-14-2010
20130174284TRANSGENIC MOUSE FOR EXPRESSING HUMAN FERRITIN IN TISSUE NON-SPECIFIC MANNER AND USE THEREOF - The present invention relates to a recombinant vector and a transgenic mouse for expressing human ferritin in a tissue non-specific manner, and more particularly, to a vector prepared by operably linking a human ferritin gene to a promoter including a cytomegalovirus (CMV) early enhancer element and a β-actin promoter, and a transgenic mouse expressing human ferritin in a tissue non-specific manner, which is transformed with the vector. Further, the present invention relates to a method for preparing a transgenic mouse, and a method for monitoring cell or tissue therapy using the transgenic mouse.07-04-2013
20090019555ANIMAL MODEL FOR CHRONIC OBSTRUCTIVE PULMONARY DISEASE AND CYSTIC FIBROSIS - A nonhuman transgenic mammal is described whose genome comprises a promoter construct operably linked to a heterologous DNA encoding an epithelial sodium channel β subunit, wherein said promoter construct directs expression of the epithelial sodium channel β subunit in lung epithelial cells of said animal, and wherein said transgenic mammal has increased lung mucus retention as compared to the corresponding wild-type mammal. The animal is useful in screening compounds for activity in treating lung diseases such as cystic fibrosis and chronic obstructive pulmonary disease.01-15-2009
20120260355Method for Evaluating Inhibitory Polynucleotide Efficiency and Efficacy - The present invention provides a method for testing the efficiency of delivering an inhibitory polynucleotide to a target cell or tissue. The invention also provides a method for testing efficiency of delivering and efficacy for an effect on tumor size of an inhibitory polynucleotide against a target gene.10-11-2012
20120260354Use of K2P Potassium Channel Activators as Antalgics - The present invention relates to treating and preventing pain. More particularly the present invention demonstrates the involvement of K2P potassium channels in the antalgic effect of morphine. The present invention therefore provides a screening method for identifying antalgics.10-11-2012
20120233714NON-HUMAN MAMMALIAN ANIMAL MODEL FOR TYPE 2 DIABETES - The present invention provides a non-human mammalian animal model for type 2 diabetes, which spontaneously develops a pathological condition similar to human type 2 diabetes of a non-obese type popular for the Japanese people. The non-human mammalian animal model for type 2 diabetes according to the present invention is deficient in a function of Cdkal1 gene on the chromosome of the β cell of the pancreas.09-13-2012
20080301821Diagnostic and Therapeutic use of a Plasma Membrane Atpase - The present invention provides a protein encoded by the ATP2B gene and discloses the differential expression of the gene coding for ATP2B proteins in specific brain regions of Alzheimer's disease patients. Based on this finding, the invention provides a method for diagnosing or prognosticating Alzheimer's disease in a subject, or for determining whether a subject is at increased risk of developing Alzheimer's disease. Furthermore, this invention provides therapeutic and prophylactic methods for treating or preventing Alzheimer's disease and related neurodegenerative disorders using the ATP2B gene and its corresponding gene products. A method of screening for modulating agents of neurodegenerative diseases is also disclosed.12-04-2008
20080301822Role of alpha1-adrenergic receptors - The present invention is directed to a transgenic non-human mammal (e.g., a rodent such as a mouse) whose genome comprises a recombinant nucleic acid sequence comprising an α12-04-2008
20110047631HEAT SHOCK PROTEIN DEFICIENCIES AS MODEL SYSTEMS FOR BRAIN PATHOLOGY AND CANCER - The invention provides non-human transgenic animals as models of neurodegenerative brain pathology, including, but not limited to, Alzheimer's disease (AD), and cancer. The non-human transgenic animals of the present invention include an exogenous DNA that reduces or eliminates the expression and/or function of a molecular chaperone, including, but not limited to heat shock protein 110 (Hsp1 10) or heat shock protein 70 (Hsp70). These non-human transgenic animals may be used in methods of screening and identifying compounds useful for the prevention and/or treatment of neurodegenerative brain pathology and/or cancer.02-24-2011
20120324593Lysyl Oxidase-Like 1 (LOXL1) and Elastogenesis - Described are methods of treating and preventing conditions associated with a loss of elastic fibers. Also provided herein are methods of screening for agents useful in treating such conditions, and animal models of conditions associated with a loss of elastic fibers.12-20-2012
20120272343STROMAL INTERACTING MOLECULE KNOCKOUT MOUSE AND USES THEREOF - This invention relates to knockout mice for the Ca10-25-2012
20120272342MOUSE ARTIFICIAL CHROMOSOME VECTOR - Disclosed is a mouse artificial chromosome vector, comprising: a natural centromere derived from a mouse chromosome; a mouse-chromosome-derived long-arm fragment formed by deleting a long-arm distal region at a mouse chromosome long-arm site proximal to the centromere; and a telomere sequence, wherein the vector is stably retained in a cell and/or tissue of a mammal. In addition, disclosed are cells or non-human animals comprising the vector, and use of the cells or non-human animals.10-25-2012
20120272341NOVEL GENE DISRUPTIONS, COMPOSITIONS AND METHODS RELATING THERETO - The present invention relates to transgenic animals, as well as compositions and methods relating to the characterization of gene function. Specifically, the present invention provides transgenic mice comprising disruptions in PRO226, PRO257, PRO268, PRO290, PRO36006, PRO363, PRO365, PRO382, PRO444, PRO705, PRO1071, PRO1125, PRO1134, PRO1155, PRO1281, PRO1343, PRO1379, PRO1380, PRO1387, PRO1419, PRO1433, PRO1474, PRO1550, PRO1571, PRO1572, PRO1759, PRO1904, PRO35193, PRO4341, PRO4348, PRO4369, PRO4381, PRO4407, PRO4425, PRO4985, PRO4989, PRO5737, PRO5800, PRO5993, PRO6017, PRO7174, PRO9744, PRO9821, PRO9852, PRO9873, PRO10196, PRO34778, PRO20233, PRO21956, PRO57290, PRO38465, PRO38683 or PRO85161 genes. Such in vivo studies and characterizations may provide valuable identification and discovery of therapeutics and/or treatments useful in the prevention, amelioration or correction of diseases or dysfunctions associated with gene disruptions such as neurological disorders; cardiovascular, endothelial or angiogenic disorders; eye abnormalities; immunological disorders; oncological disorders; bone metabolic abnormalities or disorders; lipid metabolic disorders; or developmental abnormalities.10-25-2012
20110239311Agonists of NR2F6 For Immunosupression - The present invention relates to agonists/activators of NR2F6 (nuclear orphan receptor receptor Ear2) for the treatment of a disease related to an augmented immune response. Furthermore, pharmaceutical compositions comprising said agonists/activators of NR2F6 and a pharmaceutical carrier are comprised. In a further aspect, the present invention provides for a method for identifying immunosuppressants comprising contacting a cell, tissue or a non-human animal comprising a reporter construct for NR2F6-activation with a candidate molecule, measuring the reporter signal and selecting a candidate molecule which alters the reporter signal. Furthermore, the present invention relates to non-human transgenic animals or cells or tissue derived therefrom useful in the provided methods for identifying immunosuppressants. In yet another aspect, the present invention relates to ligand-mediated reporter gene expression constructs, ligand displacement constructs, fluorescent cellular sensor fusion mutant constructs, and ligand-induced homo- and/or heterodimer constructs useful in the provided methods for identifying immunosuppressants.09-29-2011
20110239310TRANSGENIC FISH AND USES THEREOF - The present invention relates to a transgenic fish having at least one genomically integrated expression cassette containing a 5′-regulatory nucleotide sequence responsive to hormones, particularly estrogenic hormones, connected in a functional manner upstream of a nucleotide sequence encoding a reporter protein. The present invention further relates to methods of using the transgenic fish for various purposes, including, for example: (1) identifying estrogenic endocrine disruptors; (2) monitoring estrogen-like activity of test samples; (3) identifying anti-estrogenic endocrine disruptors; and (4) investigating the effects of endocrine disruptors on liver regeneration. Expression cassettes, host cells, and transgenic cells of aquatic animals are also disclosed.09-29-2011
20090106851Non-Invasive, In Vivo Fluorescent Imaging of the Nervous System In Whole Living Animal - A method is disclosed involving detecting the expression of a fluorescent protein of interest in an animal, wherein the animal is a transgenic animal having in its genome nucleic acid encoding said fluorescent protein operably linked to promoter nucleic acid from a protein that is normally expressed in the nervous system of the animal, the method comprising the step of non-invasively detecting fluorescence from said protein when expressed in said animal.04-23-2009
20120090039Immunocompromised Ungulates - Porcine animals, tissue and organs as well as cells and cell lines derived from such animals are provided that lack functional endogenous immunoglobulin loci and are deficient in immunoglobulin expression and B-cells. These animals are useful as model systems for research and for development of new pharmaceutical and biological agents. In addition, methods are provided to prepare such animals.04-12-2012
20120291145TRANSGENIC MICE OVER-EXPRESSING RECEPTOR FOR ADVANCED GLYCATION ENDPRODUCT (RAGE) IN BRAIN AND USES THEREOF - The present invention provides for a transgenic non-human animal whose cells contain a DNA sequence comprising: (a) a nerve tissue specific promoter; and (b) a DNA sequence which encodes a receptor for advanced glycation endproducts (RAGE), wherein the promoter and the DNA sequence which encodes the receptor for advanced glycation endproducts (RAGE) are operatively linked to each other and integrated in the genome of the non-human animal, and wherein said non-human animal exhibits a reduced amount of cerebral tissue infarcted following a transient middle cerebral artery occlusion compared to an identical non-human animal lacking said DNA sequence.11-15-2012
20120291146Assays of Neurodegenerative Disorders, including Frontotemporal Dementia and Amyotrophic Lateral Sclerosis - The invention relates to novel assays for the in vivo analysis of neurodegenerative diseases and the use of such assays to discover therapies capable of modulating such diseases.11-15-2012
20090083863p300 transgenic animal - The present invention relates to a transgenic animal wherein DNA encoding p300 and a promoter exerting its activity in myocardial cells are introduced, and a screening method using the same.03-26-2009
20100132056Germ Cell Marker Using Fish Vasa Gene - In order to examine whether or not a germ cell derived from a donor fish, which has been transplanted into a recipient fish of a different species by a surrogate fish technique, grows or matures in the gonad of the recipient fish, it is necessary to use, as an indicator, a trait that is specifically expressed in the germ cell and can be used to distinguish the recipient fish from the donor fish. Vasa gene, which is a germ cell-specific gene, is specific to a primordial germ cell and a spermatogonium/an oogonium, and it is not expressed in a somatic cell. In the present invention, the Vasa gene sequences of a tuna, a chub mackerel, a spotted mackerel, an eastern little tuna, and a drumfish are determined, and the expression of such gene is used as a marker for a germ cell. In addition, according to the present invention, it is possible to specifically detect only a tuna Vasa gene in Vasa gene sequences that are highly conserved in fishes, without sequencing. Thus, a tuna-derived germ cell can be reliably and simply identified in the gonad of the recipient fish. As a result, the growth or breeding of tuna can be carried out with good efficiency. Moreover, utilizing the aforementioned findings, even in a case in which not only a tuna but also another Perciformes fish is used as a donor, a germ cell derived from the donor fish can be efficiently detected from the gonad of a recipient fish of a different species.05-27-2010
20100125917TRANSGENIC NON-HUMAN MAMMAL WITH AN ONCOGENIC MUTANT OF THE c-Raf-1 GENE - The invention relates to a transgenic non-human mammal whose cells express a constitutively active oncogenic mutant of the kinase-domain of the Raf-1 gene or a protein coded by a corresponding normal allele or derivative of the A, B, or c-Raf-1 gene.05-20-2010
20130024954Human Age-Related Neurodegenerative Nematode Model and Methods - Genetically modified nematodes and methods for using the same are provided.01-24-2013
20130024955METHOD FOR DETERMINING GENOTOXICITY USING NON-FLUORESCENT PROTEINS - The present invention relates to a method for determining a genotoxicity of a test substance, comprising the steps of: (a) transforming a fish with a nucleotide sequence encoding a non-fluorescent fluorescence protein with a mutation; (b) treating a test substance to the transformed fish; and (c) measuring a fluorescence in the test substance-treated fish, wherein the fluorescence is generated by reversion of the non-fluorescent fluorescence protein to the fluorescence protein due to a back mutation of the nucleotide sequence in the test substance-treated fish. According to the present invention, MutaFish system, Zebrafish (01-24-2013
20130024953Methods of Treating Disorders Associated with Protein Aggregation - The present invention relates to methods of treatment of clinical disorders associated with protein aggregation comprising administering, to a subject, an effective amount of an anti-protein aggregate (“APA”) compound selected from the group consisting of pimozide, fluphenazine (e.g., fluphenazine hydrochloride), tamoxifen (e.g., tamoxifen citrate), taxol, cantharidin, cantharidic acid, salts thereof and their structurally related compounds. It is based, at least in part, on the discovery that each of the aforelisted compounds were able to promote degradation of aggregated ATZ protein in a 01-24-2013
20120066777TEST AGENT FOR VISCERAL OBESITY AND USE THEREOF - Disclosed are: a method for detecting (diagnosing) visceral obesity in a subject; a test agent useful for the method; a method for searching for a substance that can be used as an active ingredient for ameliorating visceral obesity; and an ameliorating agent for visceral obesity or a medicinal agent for preventing a metabolic disease developed as a result of the progression of visceral obesity. As the test agent, a polynucleotide which comprises at least 15 nucleotides and can hybridize with a nucleotide sequence for coiled-coil domain containing protein 3 (CCDC3) gene or a nucleotide sequence complementary to the nucleotide sequence under stringent conditions or an antibody capable of recognizing CCDC3 protein is used.03-15-2012
20120066776IDENTIFICATION OF A JAK2 MUTATION INVOLVED IN VAQUEZ POLYGLOBULIA - The present invention concerns the V617F variant of the protein-tyrosine kinase JAK2, said variant being responsible for Vaquez Polyglobulia. The invention also relates to a first intention diagnostic method for erythrocytosis and thrombocytosis allowing their association with myeloproliferative disorders, or to the detection of the JAK2 V617F variant in myeloproliferative disorders allowing their reclassification in a new nosological group.03-15-2012
20120066775Stresscopins and their Uses - The invention provides novel nucleic acids and polypeptides, referred to herein as stresscopin 1 and stresscopin 2, which preferentially activate the CRH-R2 receptor over the R1 receptor. Stresscopins, analogs and mimetics, and related CRH-R2 agonists suppress food intake and heat-induced edema; but do not induce substantial release of ACTH. Stresscopin also finds use in the recovery phase of stress responses, as an anti-inflammatory agent, as a hypotensive agent, as a cardioprotective agent, and in the treatment of psychiatric and anxiolytic disorders. Stresscopin nucleic acid compositions find use in identifying homologous or related proteins and the DNA sequences encoding such proteins; in producing compositions that modulate the expression or function of the protein; and in studying associated physiological pathways.03-15-2012
20080229436METHODS FOR IDENTIFYING MODULATORS OF LIFESPAN AND RESISTANCE TO OXIDATIVE STRESS - The present invention provides methods for identifying agents that increase lifespan and increase resistance to oxidative and/or electrophilic stress. Also provided are methods for identifying biomarkers of longevity or identifying pathways governing longevity in response to phosphatidylinositol 3,4,5-triphosphate signaling.09-18-2008
20110247087Regulation of endogenous gene expression in cells using zinc finger proteins - The present invention provides methods for modulating expression of endogenous cellular genes using recombinant zinc finger proteins.10-06-2011
20130174285Model Animal for Studying Hair Growth Cycle - The present invention prepared a non-human animal in which Fgf18 gene was knocked out in a keratin-5 positive cell-specific manner using a Cre-loxP system; it provides a non-human model animal in which FGF18 expression has been inhibited in a hair follicle-specific manner to shorten the telogen phase of hair growth cycle. The non-human model animal is useful in studying hair follicles and skin, particularly hair growth occurring cyclically in hair follicle cells, and is applicable to the development of and screening for novel drugs against hair follicle or skin disorders.07-04-2013
20080222738Transgenic Non-Human Animal for Use in Research Models for Studying Parkinson's Disease - The invention relates to a transgenic mouse model with deficient respiratory chain function in dopamine (DA) neurons. By suppressing or deleting the mitochondrial transcription factor A (Tfam) in DA neurons, a mouse model is obtained, which reproduces key pathophysiological features of Parkinson's disease (PD), i.e., slow progressive loss of DA terminals in striatum and loss of DA neurons in substantia nigra pars compacta; alpha-synuclein immunoreactivity including intracellular inclusions similar to Lewy bodies in affected areas prior to and during cell loss; progressive movement disorder associated with abnormal gait, tremor and rigid limbs. The mouse model can be used to develop pharmacological, gene therapy or cell therapy treatments for PD.09-11-2008
20130179998TRANSGENIC MOUSE MODEL EXPRESSING AMYLOID BETA 4-42 PEPTIDE - The present invention describes a novel transgenic mouse model for the common sporadic form of Alzheimer's disease. More particularly, the invention relates to a nucleotide sequence encoding Aβ 4-42 in functional linkage with at least a promoter, signal peptide sequence and a polyadenylation signal sequence, a cell and a transgenic non-human animal comprising said nucleotide sequence, and their respective use in screening methods.07-11-2013
20130179997TRANSGENIC ANIMAL EXPRESSING ALZHEIMER'S TAU PROTEIN - The present invention provides transgenic non-human animals and non-human mammalian somatic and germ cells harbouring a human DNA sequence encoding Alzheimer's Disease (AD) derived tau protein, capable of inducing AD pathology in transgenic animals. Alzheimer's tau protein is expressed on specific genetic backgrounds allowing also simulation of different human diseases including hypertension, diabetes, hyper-cholesterolemia, which are associated with neurodegeneration and are considerable risk factors for AD development. Transgenic animals and cells of the invention exhibit neurofibrillary pathology and may serve as in vivo and in vitro assay systems for screening and developing therapeutic and preventive substances and also diagnostic markers and probes for tauopathies and AD. Furthermore these transgenic animals and cell lines derived thereof provide an in vivo and in vitro assay system for neurodegenerative disorders preferably tauopathies and AD result from combinations with other disease as hypertension and others representing risk factors associated with the process of neurodegeneration.07-11-2013
20120255041TRANSGENIC NON-HUMAN ANIMAL AND USES THEREOF - The present invention relates generally to transgene constructs, transgenic non-human animals comprising transgene constructs, methods of making and methods of using the transgenic non-human animals comprising transgene constructs. An embodiment of the invention relates to methods of assaying the activation of GPCR ligands non-invasively in whole animals, tissue slices, or in native cells using a transgenic model containing a bioluminescent transgene reporter system that is responsive to pathway modulation following ligand binding of GPCR receptors.10-04-2012
20130091591ARTERY- AND VEIN-SPECIFIC PROTEINS AND USES THEREFOR - Arterial and venous endothelial cells are molecularly distinct from the earliest stages of angiogenesis. This distinction is revealed by expression on arterial cells of a transmembrane ligand, called EphrinB2 whose receptor EphB4 is expressed on venous cells. Targeted disruption of the EphrinB2 gene prevents the remodeling of veins from a capillary plexus into properly branched structures. Moreover, it also disrupts the remodeling of arteries, suggesting that reciprocal interactions between pre-specified arterial and venous endothelial cells are necessary for angiogenesis. This distinction can be used to advantage in methods to alter angiogenesis, methods to assess the effect of drugs on artery cells and vein cells, and methods to identify and isolate artery cells and vein cells, for example.04-11-2013
20100281548Animal models for demyelination disorders - This invention is in the field of neurology. Specifically, the invention relates to the discovery and characterization of molecular components that play a role in neuronal demyelination or remyelination. In addition, the invention relates to the generation of an animal model that exhibits hypomyelination. The compositions and methods embodied in the present invention are particularly useful for drug screening and/or treatment of demyelination disorders.11-04-2010
20080201786Transgenic Zebrafish Models of Alzheimer's Disease - The present invention relates to zebrafish models for Alzheimer's disease that allow recapitulation of pathologies associated with Alzheimer's disease. This invention also relates to methods for screening of compounds for their ability to modulate a pathology associated with Alzheimer's disease in vivo in a whole vertebrate organism. The present invention further relates to methods of identifying gene targets for compounds that modulate a pathology associated with Alzheimer's disease.08-21-2008
20110239312METHODS OF DIAGNOSING AND TREATING MOTOR NEURON DISEASES - Use of an agent which upregulates an activity or amount of miRNA-9 or miRNA-9* is disclosed for the preparation of a medicament for the treatment of a motor neuron disease (MND).09-29-2011
20130152222TRANSGENIC FISH AND USES THEREOF - The present invention relates to a transgenic fish having at least one genomically integrated expression cassette containing a 5′-regulatory nucleotide sequence responsive to hormones, particularly estrogenic hormones, connected in a functional manner upstream of a nucleotide sequence encoding a reporter protein. The present invention further relates to methods of using the transgenic fish for various purposes, including, for example: (1) identifying estrogenic endocrine disruptors; (2) monitoring estrogen-like activity of test samples; (3) identifying anti-estrogenic endocrine disruptors; and (4) investigating the effects of endocrine disruptors on liver regeneration. Expression cassettes, host cells, and transgenic cells of aquatic animals are also disclosed.06-13-2013
20100299767TREM-2 GENE AND PROTEIN AS INHIBITORS OF EXPRESSION OF GA733-2, AND TRANSGENIC ANIMALS COMPRISING THE SAME AND USES THEREOF - Disclosed are a composition for inhibiting the expression of GA733-2 or for detecting GA733-2, which comprises TREM-2 gene or protein, a transgenic animal containing same, and a method using the same.11-25-2010
20100319075STG Promoter And Its Use As A Marker For Taste And Oocyte Cells - The present invention relates to a polynucleotide vector comprising the Simian taste-bud specific gene (STG) promoter operatively linked to a reporter gene. In preferred embodiments, the STG promoter is the murine ortholog of the STG promoter. In other preferred embodiments, the STG promoter is the human ortholog of the STG promoter. In some preferred embodiments, the reporter gene is green fluorescent protein (GFP). Additionally provided are vectors comprising the STG promoter operatively linked to a cre-recombinase gene.12-16-2010
20100319074MULTI-TARGETED RNAI THERAPEUTICS FOR SCARLESS WOUND HEALING OF SKIN - The present invention provides small interfering RNA (siRNA) molecules, compositions containing them, and methods of using them for improvement of skin scarless wound healing and other skin conditions, such as psoriasis and lupus-caused cutaneous lesions. The invention includes siRNA molecules and compositions containing them that inhibit the expression of one or more genes that promote pathological or undesired processes in wound healing and methods of using them.12-16-2010
20100319073GDE Compositions and Methods - The present invention relates to compositions to treat glycerophosphodiester phosphodiesterase (GDE) related disorders. The invention also relates to methods treating GDE related disorders. The invention further relates to kits for treating GDE related disorders in a subject. The invention further relates to methods of identifying novel treatments for treating GDE related disorders in a subject.12-16-2010
20120284809KNOCK DOWN MODEL OF DICKKOPF HOMOLOGUE 3 (Dkk3) FOR ASSESSING ROLE OF SAID Dkk3 IN SPERMATOGENESIS AND SEX REVERSAL - The present invention relates the function of Dickkopf 3 (Dkk3 ) in testis using shRNA mediated knock down model. Specifically, the present invention provides knock down model comprising reduction in Dkk3 activity. The knock down model of Dkk3 consisting of non human vertebrates which have, incorporated in their genome, shRNA construct targeting mammalian Dkk3 gene exhibits low testis weight, low sperm count and has low litter size. The knock down model displays disrupted seminiferous tubules and are subfertile. The present invention model has a role in sex determination as its interruption leads to sex reversal of XY gonads, converting males to females. Sex reversal role of Dkk3 knock down model can find its utility in agricultural applications. The present invention describes Dkk3 as a dual function protein which is associated with sex determination as well as is essential for the process of spermatogenesis. Such testicular functional studies are useful as a model for various disease states of infertility or subfertility and for identifying a potential treatment to overcome idiopathic infertility.11-08-2012
20130160151TRANSGENIC ANIMAL AS A MODEL FOR IDENTIFYING ADULT STEM CELLS, AND USES THEREOF - The present invention relates to the use of a transgenic non-human animal, such as a mouse, expressing a reporter gene detectable by a chromogenic, luminescent or fluorescent signal which identifies the cells that express Pw1, or of Pw1-expressing cells or tissues isolated therefrom, as a model for screening a candidate substance for its ability to stimulate adult stem cells, or for monitoring cell aging.06-20-2013
20090094703Novel medulloblastoma-forming cell line - Isolated medulloblastoma-forming clonogenic cells are provided which are useful to form stable cell lines as well as a non-human animal models of medulloblastoma that mimic human medulloblastoma, thereby providing a means to screen for candidate therapeutic compounds.04-09-2009
20110283370MOUSE MODEL FOR DEPRESSION, SCHIZOPHRENIA AND ALZHEIMER'S DISEASE AND THE USE THEREOF - The present invention relates to Glycine N-methyltransferase (GNMT) animal model and use thereof.11-17-2011
20110321179NON-HUMAN ANIMAL MODEL FOR AMYOTROPHIC LATERAL SCLEROSIS (ALS) WITH LOSS-OF-TDP-43 FUNCTION - A non-human animal model for amyotrophic lateral sclerosis (ALS) is disclosed. The animal model comprises a rodent whose spinal cord motor neurons have a loss of TAR-DNA binding protein-43 (TDP-43) function and phenotypes exhibit ALS-like symptoms. A method for identifying a candidate agent for treating, preventing and/or inhibiting ALS associated with a loss-of-function of TDP-43 is also disclosed.12-29-2011
20130191931FUMARYLACETOACETATE HYDROLASE (FAH)-DEFICIENT PIGS AND USES THEREOF - Described herein is the generation of Fah07-25-2013
20120030777METHODS FOR TESTING FOR CALORIC RESTRICTION (CR) MIMETICS - Methods for treating neurological diseases and for testing Caloric Restriction (CR) mimetics or CR mimetic candidates. In one exemplary method, a CR mimetic candidate is administered to a transgenic animal and the effects of the administering are determined; the transgenic animal includes an added gene from another type of animal or a modified gene which is designed to produce a disease or ailment of another type of animal, and the method seeks to determine whether the CR mimetic candidate improves the disease or ailment. Methods relating to neurological disease and other methods relating to CR mimetic testing are also described.02-02-2012
20120030778GENOMIC EDITING OF GENES INVOLVED WITH PARKINSONS DISEASE - The present invention provides genetically modified animals and cells comprising edited chromosomal sequences encoding proteins associated with Parkinson's disease. In particular, the animals or cells are generated using a zinc finger nuclease-mediated editing process. Also provided are methods of assessing the effects of agents in genetically modified animals and cells comprising edited chromosomal sequences encoding proteins associated with Parkinson's disease.02-02-2012
20120030776NOVEL GENE DISRUPTIONS, COMPOSITIONS AND METHODS RELATING THERETO - The present invention relates to transgenic animals, as well as compositions and methods relating to the characterization of gene function. Specifically, the present invention provides transgenic mice comprising disruptions in PRO69122, PRO204, PRO214, PRO222, PRO234, PRO265, PRO309, PRO332, PRO342, PRO356, PRO540, PRO618, PRO944, PRO994, PRO1079, PRO1110, PRO1122, PRO1138, PRO1190, PRO1272, PRO1286, PRO1295, PRO1309, PRO1316, PRO1383, PRO1384, PRO1431, PRO1434, PRO1475, PRO1481, PRO1568, PRO1573, PRO1599, PRO1604, PRO1605, PRO1693, PRO1753, PRO1755, PRO1777, PRO1788, PRO1864, PRO1925, PRO1926, PRO3566, PRO4330, PRO4423, PRO36935, PRO4977, PRO4979, PRO4980, PRO4981, PRO5801, PRO5995, PRO6001, PRO6095, PRO6182, PRO7170, PRO7171, PRO7436, PRO9912, PRO9917, PRO37337, PRO37496, PRO19646, PRO21718, PRO19820, PRO21201, PRO20026, PRO20110, PRO23203 or PRO35250 genes. Such in vivo studies and characterizations may provide valuable identification and discovery of therapeutics and/or treatments useful in the prevention, amelioration or correction of diseases or dysfunctions associated with gene disruptions such as neurological disorders; cardiovascular, endothelial or angiogenic disorders; eye abnormalities; immunological disorders; oncological disorders; bone metabolic abnormalities or disorders; lipid metabolic disorders; or developmental abnormalities.02-02-2012
20130198874Model Animal for Pregnancy-induced Hypertension Syndrome, and Treatment Method Therefor - A lentiviral vector was used to produce non-human animals that express human sFLT1 specifically in the murine placenta, to provide model animals of diseases such as pregnancy-induced hypertension syndrome that are close to the clinical conditions, methods for producing the model animals, methods of screening for candidate compounds as therapeutic agents for diseases such as pregnancy-induced hypertension syndrome by using the model animals, and therapeutic agents for diseases such as pregnancy-induced hypertension syndrome. As a result, the model animals were found to exhibit symptoms that are very close to the clinical conditions in human, which are presentation of hypertension as well as placental insufficiency, intrauterine growth retardation, glomerulosclerosis, and proteinuria during pregnancy, and improvement of those symptoms postpartum. Furthermore, when pravastatin was administered to this model animal, it was found that diseases such as pregnancy-induced hypertension syndrome were improved by the activation of placenta-derived growth factor (PIGF) which antagonizes sFLT1.08-01-2013
20120096568TRANSGENIC LSD1 ANIMAL MODEL FOR CANCER - The present invention relates to a non-human transgenic animal whose genome comprises a stably integrated transgenic nucleotide sequence encoding Lysine-specific Demethylase 1 (LSD1) operably linked to a promoter. The invention further concerns methods for generating the non-human animal and its use as a cancer model.04-19-2012
20130212715Biomarkers for Hematologic Malignacies - It has been discovered that STAT5 phosphorylation and CD150 are effective biomarkers for detecting, diagnosing, and monitoring hematological malignancies, including for example lymphomas. Compositions and methods for identifying therapeutic agents for the treatment of hematologic malignancies using p-STAT5, CD150 or both as biomarkers are described.08-15-2013
20130212716PFKs as Modifiers of the IGFR Pathway and Methods of Use - Human PFK genes are identified as modulators of the IGFR pathway, and thus are therapeutic targets for disorders associated with defective IGFR function. Methods for identifying modulators of IGFR, comprising screening for agents that modulate the activity of PFK are provided.08-15-2013

Patent applications in class METHOD OF USING A TRANSGENIC NONHUMAN ANIMAL IN AN IN VIVO TEST METHOD (E.G., DRUG EFFICACY TESTS, ETC.)