Cell death signal transduction and Bcl-2 function

Biochem Soc Trans. 1996 Nov;24(4):1059-65. doi: 10.1042/bst0241059.


The mechanism by which Bcl-2 can insulate cells against multiple diverse apoptotic signals is largely undefined. How is it possible that Bcl-2, which possesses no known catalytic function, can protect against multiple cell-death signals? A proposal to address this question postulates that Bcl-2 functions at convergence points common to most cell-death signal-transduction pathways. This review attempts to integrate observations regarding cell-death signalling in an effort to define points of convergence. The ceramide/ SAPK/JNK and NF kappa B pathways, in particular, were emphasized. Potential points at which Bcl-2 may function frequently involve the transmembrane trafficking of molecules implicated in the mediation of apoptosis. The selectivity of this process and the effector proteins with which Bcl-2 associated remain to be elucidated.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Apoptosis*
  • Cell Compartmentation
  • Ceramides / physiology
  • Genes, bcl-2*
  • Humans
  • Models, Biological
  • NF-kappa B / metabolism
  • Oxidative Stress
  • Signal Transduction*
  • Tumor Necrosis Factor-alpha / pharmacology


  • Ceramides
  • NF-kappa B
  • Tumor Necrosis Factor-alpha