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Regulation of CDK4 activity by a novel CDK4-binding protein, p34(SEI-1).

Genes & development | Nov 15, 1999

The p16(INK4a) tumor suppressor inhibits cyclin-dependent kinases (CDK4 and CDK6). Here we report the isolation of a novel gene, SEI-1, whose product (p34(SEI-1)) appears to antagonize the function of p16(INK4a). Addition of p34(SEI-1) to cyclin D1-CDK4 renders the complex resistant to inhibition by p16(INK4a). Expression of SEI-1 is rapidly induced on addition of serum to quiescent fibroblasts, and ectopic expression of p34(SEI-1) enables fibroblasts to proliferate even in low serum concentrations. p34(SEI-1) seems to act as a growth factor sensor and may facilitate the formation and activation of cyclin D-CDK complexes in the face of inhibitory levels of INK4 proteins.

Pubmed ID: 10580009 RIS Download

Mesh terms: Animals | Blood Physiological Phenomena | COS Cells | Carrier Proteins | Cell Cycle | Cells, Cultured | Cercopithecus aethiops | Chromosomes, Human, Pair 19 | Culture Media, Serum-Free | Cyclin-Dependent Kinase 4 | Cyclin-Dependent Kinase Inhibitor p16 | Cyclin-Dependent Kinases | DNA, Complementary | Enzyme Activation | Fibroblasts | Genes | HeLa Cells | Humans | Nuclear Proteins | Proto-Oncogene Proteins | Saccharomyces cerevisiae | Trans-Activators | Transfection | Two-Hybrid System Techniques

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