p202 prevents apoptosis in murine AKR-2B fibroblasts

Dimpy Koul, Ruth Lapushin, Hong Ji Xu, Gordon B. Mills, Jordan U. Gutterman, Divaker Choubey

    Research output: Contribution to journalArticle

    29 Scopus citations

    Abstract

    p202 is an interferon (IFN)-inducible, primarily nuclear, phosphoprotein (52-kDa) whose overexpression in transfected cells inhibits colony formation. p202 binds to the retinoblastoma tumor suppressor protein and two other members of the pocket family proteins (p107 and p130). Moreover, overexpression of p202 in transfected cells inhibits the transcriptional activity of E2Fs (E2F-1/DP-1 and E2F-4/DP-1), p53, AP-1 c-Fos and c-Jun, NF-κB p50 and p65. Here we demonstrate that inhibition of endogenous p202 production in murine AKR-2B fibroblasts did not result in an increase in cell proliferation. Instead, these cells exhibited increased susceptibility to apoptosis in response to decrease in serum concentrations in the growth medium. These observations are consistent with the notion that normal levels of p202 may be needed for the regulation of cell proliferation.

    Original languageEnglish (US)
    Pages (from-to)379-382
    Number of pages4
    JournalBiochemical and Biophysical Research Communications
    Volume247
    Issue number2
    DOIs
    StatePublished - Jun 18 1998

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    ASJC Scopus subject areas

    • Biophysics
    • Biochemistry
    • Molecular Biology
    • Cell Biology

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