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

M. L. Helms, A. A. A. Mohamed, D. J. 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 pages7
JournalFEBS Letters
Volume505
Issue number1
Publication statusPublished - 2001

Keywords

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

Cite this