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

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    Authors
    Sugimoto, Masataka
    Nakamura, Takeshi
    Ohtani, Naoko
    Hampson, Lynne
    Hampson, Ian N
    Shimamoto, Akira
    Furuichi, Yasuhiro
    Okumura, Ko
    Niwa, Shinichiro
    Taya, Yoichi
    Hara, Eiji
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    Affiliation
    Paterson Institute for Cancer Research, Christie Hospital National Health Service Trust, Manchester, M20 4BX, UK.
    Issue Date
    1999-11-15
    
    Metadata
    Show full item record
    Abstract
    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.
    Citation
    Regulation of CDK4 activity by a novel CDK4-binding protein, p34(SEI-1). 1999, 13 (22):3027-33 Genes Dev.
    Journal
    Genes & Development
    URI
    http://hdl.handle.net/10541/91374
    PubMed ID
    10580009
    Type
    Article
    Language
    en
    ISSN
    0890-9369
    Collections
    All Paterson Institute for Cancer Research

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