PMID: 9446703Apr 4, 1998Paper

Cellular stimulation via CD95 involves activation of phospho-inositide-3-kinase

Pflügers Archiv : European journal of physiology
E GulbinsF Lang

Abstract

Several distinct intracellular pathways have been recently shown to be activated during CD95/Fas/APO-1-mediated apoptosis. Here, we demonstrate that CD95 ligation induces a rapid and transient tyrosine phosphorylation and activation of phosphoinositide-3-kinase (PI-3-K) in Jurkat T lymphocytes or CD95-sensitive glioma cells. Experiments using p56lck-deficient or p56lck-reconstituted Jurkat clones and the tyrosine kinase inhibitor herbimycin A revealed that tyrosine phosphorylation and activation of PI-3-K by CD95 depends on expression of Src-like tyrosine kinases, in particular p56lck. PI-3-K stimulation seems to be critical for CD95 receptor signalling since, first, inhibition of PI-3-K prevents CD95-mediated apoptosis and, second, CD95 receptor ligation fails to induce tyrosine phosphorylation or activation of PI-3-K in CD95-resistant glioma cells. Thus, PI-3-K activation may be an early signalling event during CD95-induced apoptosis, and failure to stimulate PI-3-K may predict tumor cell resistance to CD95-triggered apoptosis.

Citations

Oct 2, 2003·Journal of Molecular and Cellular Cardiology·Mark ShilkrutOfer Binah
Feb 11, 2003·Pharmacology & Therapeutics·Angela ClerkDonna M Valks
Feb 16, 2005·Annual Review of Physiology·Wolfgang Neuhofer, Franz-X Beck
Apr 19, 2013·Scandinavian Journal of Immunology·N-H ChenA-Y Lee
Mar 11, 2008·Cancer Cell·Susanne KleberAna Martin-Villalba
Dec 26, 2001·The Journal of Biological Chemistry·Vladimir N IvanovZe'ev Ronai
May 20, 2006·The Journal of Immunology : Official Journal of the American Association of Immunologists·Bin LuYon Rojanasakul
Aug 23, 2011·The Journal of Immunology : Official Journal of the American Association of Immunologists·Anand Krishnan V IyerYon Rojanasakul

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