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    Opposing effects of Ets and Id proteins on p16INK4a expression during cellular senescence.

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    Authors
    Ohtani, Naoko
    Zebedee, Zoe
    Huot, Thomas J G
    Stinson, Julie A
    Sugimoto, Masataka
    Ohashi, Yasuhiro
    Sharrocks, Andrew D
    Peters, Gordon
    Hara, Eiji
    Affiliation
    Paterson Institute for Cancer Research, Christie Hospital NHS Trust, Manchester, UK.
    Issue Date
    2001-02-22
    
    Metadata
    Show full item record
    Abstract
    The p16INK4a cyclin-dependent kinase inhibitor is implicated in replicative senescence, the state of permanent growth arrest provoked by cumulative cell divisions or as a response to constitutive Ras-Raf-MEK signalling in somatic cells. Some contribution to senescence presumably underlies the importance of p16INK4a as a tumour suppressor but the mechanisms regulating its expression in these different contexts remain unknown. Here we demonstrate a role for the Ets1 and Ets2 transcription factors based on their ability to activate the p16INK4a promoter through an ETS-binding site and their patterns of expression during the lifespan of human diploid fibroblasts. The induction of p16INK4a by Ets2, which is abundant in young human diploid fibroblasts, is potentiated by signalling through the Ras-Raf-MEK kinase cascade and inhibited by a direct interaction with the helix-loop-helix protein Id1 (ref. 11). In senescent cells, where the Ets2 levels and MEK signalling decline, the marked increase in p16INK4a expression is consistent with the reciprocal reduction of Id1 and accumulation of Ets1.
    Citation
    Opposing effects of Ets and Id proteins on p16INK4a expression during cellular senescence. 2001, 409 (6823):1067-70 Nature
    Journal
    Nature
    URI
    http://hdl.handle.net/10541/85725
    DOI
    10.1038/35059131
    PubMed ID
    11234019
    Type
    Article
    Language
    en
    ISSN
    0028-0836
    ae974a485f413a2113503eed53cd6c53
    10.1038/35059131
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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