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

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

Authors

  • Sugimoto M
  • Nakamura T
  • Ohtani N
  • Hampson L
  • Hampson IN
  • Shimamoto A
  • Furuichi Y
  • Okumura K
  • Niwa S
  • Taya Y
  • Hara E

Journal

Genes & development

Publication Data

November 15, 1999

Associated Grants

None

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