PMID: 9164843May 15, 1997Paper

Bcl-2 does not require Raf kinase activity for its death-protective function

The Biochemical Journal
R OlivierC Borner

Abstract

It has been widely accepted that the oncogene product bcl-2 protects mammalian cells from programmed cell death (apoptosis). The molecules and signalling pathways upon which bcl-2 acts are, however, still ill-defined. Recently, bcl-2 was shown to interact with c-raf-1 in vitro. Furthermore, an active form of c-raf-1 delayed apoptosis induced by trophic factor deprivation and enhanced the death-suppressive function of bcl-2 when co-expressed. This has led to the hypothesis that bcl-2 communicates cell-death protection via a raf-dependent signal transduction pathway. Here we show, by various immunological and biochemical methods, that bcl-2 does not stably associate with c-raf-1 in cellular extracts prepared from fibroblasts before or after treatment with agents that induce apoptosis. Unexpectedly, bcl-2 function is entirely maintained, if not improved, when raf-dependent signalling is experimentally abrogated. In fact, bcl-2 allows the stable overexpression of a kinase-defective dominant-negative raf mutant that usually interferes with cell viability and/or proliferation. Our results indicate that bcl-2 does not require c-raf-1 kinase activity and an associated mitogen-activated protein kinase signalling pathway for its survival...Continue Reading

Citations

Apr 16, 1998·The Journal of Biological Chemistry·L MonneyC Borner
May 31, 2007·The Journal of Biological Chemistry·Sem KebacheAndré Nantel
Feb 5, 2008·Oncogene·K Boisvert-Adamo, A E Aplin
May 5, 2001·Pharmacology & Therapeutics·C R Weinstein-OppenheimerJ A McCubrey
Apr 8, 1998·Current Opinion in Genetics & Development·J Downward

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