Disruption of the ARF transcriptional activator DMP1 facilitates cell immortalization, Ras transformation, and tumorigenesis

Article Abstract:

The DMP1 gene, the ARF transcriptional activator in mice, has been disrupted, with the result that CMP1 loss of function was found to mimic key aspects of the ARF-null phenotype. The disruption was helpful to Ras transformation, cell immortalization, and tumorigenesis. It seems that ARF function is inhibited, but not gone, in animals that do not have functional DMP1.

author: Inoue, Kazushi, Wen, Renren, Rehg, Jerold E., Adachi, Masashi, Cleveland, John L., Roussel, Martine F., Sherr, Charles J.
Cell death, Cell cycle, Carcinogenesis, Ras genes

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p53-independent functions of the p19(super.ARF) tumor suppressor

Article Abstract:

The p19(super.ARF) tumor suppressor and its p53-independent functions are discussed. Mice nullizygous for p53, ARF and Mdm2 were generated. Reintroducing ARF in cells without its only known target and the effects thereof were investigated. ARF-p53-Mdm2 appears to have a pathway that is not entirely straightforward. Where there is no Mdm2, p10ARF has been seen to interact with other targets to inhibit cell proliferation.

author: Lozano, Guillermina, Rehg, Jerold E., Roussel, Martine F., Sherr, Charles J., Weber, Jason D., Jeffers, John R., Randle, David H., Zambetti, Gerard P.
Cellular signal transduction, Tumors, Cell proliferation

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Dmp1 is haplo-insufficient for tumor suppression and modifies the frequencies of Arf and p53 mutations in Myc-induced lymphomas

Article Abstract:

Dmp1, an Arf transcriptional activator, is haplo-insufficient for tumor suppression and alters frequencies of p53 and Arf mutations in Myc-induced lymphoma according to this research communication article. Loss of Dmp1 leads to spontaneous tumorigenesis in mice, bringing cancer death by age two years.

author: Rehg, Jerold E., Sherr, Charles J., Randle, David H., Inour, Kazushi, Zindy, Frederique
Health aspects, Lymphomas

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subjects list: Statistical Data Included, Research, United States, Usage, Physiological aspects, Cytochemistry, Mice, mutant strains, Mutant mice, Tumor suppressor genes, Genetic aspects
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