Non-apoptotic Fas signaling

Cytokine Growth Factor Rev. 2003 Feb;14(1):53-66. doi: 10.1016/s1359-6101(02)00072-2.

Abstract

Fas (Apo-1, CD95) and Fas-Ligand (FasL, CD95L) are typical members of the TNF receptor and TNF ligand family, respectively, with a pivotal role in the regulation of apoptotic processes, including activation-induced cell death, T-cell-induced cytotoxicity, immune privilege and tumor surveillance. Impairment of the FasL/Fas system has been implicated in liver failure, autoimmune diseases and immune deficiency. Thus, the FasL/Fas system was mainly appreciated with respect to its death-inducing capabilities. However, there is increasing evidence that activation of Fas can also result in non-apoptotic responses like cell proliferation or NF-kappaB activation. While the apoptotic features of the FasL/Fas system and the pathways involved are comparably well investigated, the pathways that are utilized by Fas to transduce proliferative and activating signals are poorly understood. This review is focused on the non-apoptotic functions of the FasL/Fas system. In particular, the similarities and differences of the molecular mechanisms of apoptotic and non-apoptotic Fas signaling are addressed.

Publication types

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

MeSH terms

  • Animals
  • Apoptosis / physiology*
  • Cell Differentiation / physiology
  • Cell Division / physiology
  • Enzyme Activation
  • Fas Ligand Protein
  • Humans
  • Inflammation / metabolism
  • JNK Mitogen-Activated Protein Kinases
  • Membrane Glycoproteins / metabolism
  • Mitogen-Activated Protein Kinases / metabolism
  • NF-kappa B / metabolism
  • Signal Transduction / physiology*
  • fas Receptor / metabolism*

Substances

  • FASLG protein, human
  • Fas Ligand Protein
  • Membrane Glycoproteins
  • NF-kappa B
  • fas Receptor
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases