Article Abstract:
Genes controlling the G(sub.2)/M checkpoint and cooperative effects they have are discussed. Results show p21 and 14-3-3(sigma) have complementary roles in the G2/M checkpoint. Human cells deficient in p21 and 14-3-3(sigma) were generated. Study was made of whether the double knockout was more sensitive to DNA damage than either one of the single knockouts. Results of the study contribute to understanding of why genes at the nodal points of growth-arrest pathways, such as p53, are targeted for mutation in cancer cells. Multiple effectors are thought to independently control the checkpoints allowing transition between cell cycle phases, but in mammal cells this has not been shown definitively.
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Article Abstract:
Cyclin-dependent kinase (CDK) inhibitors (CKIs) are positive and negative regulators of first gap phase (G(sub.1)-phase) progression. CKIs are required for cyclin D-CDK assembly and INK4 proteins are dependent on Cip/Kip proteins to bring on G(sub.1)-phase arrest. The major role of the D-type cylins is as growth factor sensors. They convert environmental signals to fuel to run the cell cycle engine. The necessity of cyclin D-dependent kinase activity for the cell cycle and a role for Cip/Kip proteins in cancer are discussed and current literature is reviewed.
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Article Abstract:
PPAR delta, which is in the nuclear receptor superfamily, is discussed as an APC-regulated target of nonsteroidal anti-inflammatories (NSAIDs). PPAR delta was found to be a target of APC in analysis of global gene expression profiles in human colorectal cancer cells. It is likely that NSAIDs inhibit tumorigenesis by inhibition of PPAR delta. Its gene is usually regulated by APC.
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