Modulated kinase activities in cells undergoing tumour necrosis factor-induced apoptotic cell death

M. J. Helms, Ahmed Mohamed, David Joseph MacEwan

    Research output: Contribution to journalArticle

    11 Citations (Scopus)

    Abstract

    Tumour necrosis, factor-alpha (TNF) has, a variety of cellular effects including apoptotic, and necrotic cytotoxicity. TNF activates a range of kinases, but their role in cytotoxic mechanisms is unclear. HeLa cells expressing elevated type II 75 kDa TNF receptor (TNFR2) protein, analysed by flow cytometry and Western analysis, showed altered c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38MAPK; but not MAPK) protein content and activation. There was greater JNK activation, but reduced p38MAPK activation in dying cells compared to those still to enter TNF-induced apoptosis. Moreover, cells displaying more rapid apoptosis possess higher levels of type I 55 kDa TNFR1 receptor isoform, but less TNFR2. These findings reveal differential kinase activation in TNF-induced apoptotic death. (C) 2001 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.

    Original languageEnglish
    Pages (from-to)68-74
    Number of pages6
    JournalFEBS Letters
    Volume505
    Issue number1
    DOIs
    Publication statusPublished - 2001

    Keywords

    • cytokine
    • receptor
    • subtype
    • signal transduction
    • kinase
    • tumor
    • ACTIVATED PROTEIN-KINASE
    • N-TERMINAL KINASE
    • CYTOSOLIC PHOSPHOLIPASE A(2)
    • FACTOR-ALPHA
    • TNF RECEPTOR
    • SIGNAL-TRANSDUCTION
    • JNK ACTIVATION
    • PHORBOL ESTER
    • CYTOCHROME-C
    • HELA-CELLS

    Cite this