p38/RK is essential for stress-induced nuclear responses: JNK/SAPKs and c-Jun/ATF-2 phosphorylation are insufficient

Catherine A. Hazzalin, Eva Cano, Ana Cuenda, Michael J. Barratt, Philip Cohen, Louis C. Mahadevan

    Research output: Contribution to journalArticle

    195 Citations (Scopus)

    Abstract

    The ERK, JNK/SAPK and p38/RK MAP kinase subtypes (reviewed in [1]) are differentially activated in mammalian cells by various stimuli, which elicit induction of immediate-early (IE) genes, such as c-fos and c-jun (reviewed in [1-3]), as well as phosphorylation of histone H3 [4] and HMG-14 [5]. Anisomycin and UV radiation have been suggested to induce c-fos and c-jun transcription via JNK/SAPK-mediated phosphorylation of TCF (ternary complex factor), for c-fos induction [6-8], and c-jun and/or ATF-2 for c-jun induction [9-13]. We report here that anisomycin and ultraviolet radiation (UV) activate MAP kinase kinase-6 (MKK6) [14,15], p38/RK [16-18] and MAPKAP kinase-2 (MAPKAP K-2) [17-19]. By using the p38/RK inhibitor SB 203580 [20,21], we show that activation of p38/RK and/or its downstream effectors are essential for anisomycin- and UV-stimulated c-fos/c-jun induction and histone H3/HMG-14 phosphorylation, whereas JNK/SAPK activation and phosphorylation of c-jun and ATF-2 are insufficient for these responses.

    Original languageEnglish
    Pages (from-to)1028-1031
    Number of pages4
    JournalCurrent Biology
    Volume6
    Issue number8
    DOIs
    Publication statusPublished - Aug 1996

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