Fas ligand-induced apoptosis

Annu Rev Genet. 1999;33:29-55. doi: 10.1146/annurev.genet.33.1.29.

Abstract

The immune response is regulated not only by cell proliferation and differentiation, but also by programmed cell death, or apoptosis. In response to various stimuli, death factors bind to their respective receptors and activate the apoptotic death program in target cells. A cascade of specific proteases termed caspases mediates the apoptotic process. The activated caspases cleave various cellular components, a process that leads to morphological changes of the cells and nuclei, as well as to degradation of the chromosomal DNA. Loss-of-function mutations in the signaling molecules involved in apoptosis cause hyper-proliferation of cells in mouse and human. In contrast, exaggeration of this death cascade causes the destruction of various tissues.

Publication types

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

MeSH terms

  • Animals
  • Apoptosis*
  • Chromosomes / physiology*
  • DNA / genetics
  • Fas Ligand Protein
  • Humans
  • Membrane Glycoproteins / physiology*
  • Mice
  • fas Receptor / physiology*

Substances

  • FASLG protein, human
  • Fas Ligand Protein
  • Fasl protein, mouse
  • Membrane Glycoproteins
  • fas Receptor
  • DNA