Signaling and transcriptional control of Fas ligand gene expression

Cell Death Differ. 2003 Jan;10(1):36-44. doi: 10.1038/sj.cdd.4401179.


Fas ligand (FasL), a member of the tumor necrosis factor family, initiates apoptosis by binding to its surface receptor Fas. As a consequence, there is sequential activation of caspases and the release of cytochrome c from the mitochondria, with additional caspase activation followed by cellular degradation and death. Recent studies have shed important insight into the molecular mechanisms controlling FasL gene expression at the level of transcription. Nuclear factors such as nuclear factor in activated T cells, nuclear factor-kappa B, specificity protein-1, early growth response factor, interferon regulatory factor, c-Myc and the forkhead transcriptional regulator, alone or cooperatively, activate FasL expression. These factors are often coexpressed with FasL in pathophysiologic settings including human atherosclerotic lesions. Here, we review these important advances in our understanding of the signaling and transcriptional mechanisms controlling FasL gene expression.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis / genetics
  • Apoptosis / immunology*
  • Cytokines / genetics
  • Cytokines / immunology
  • Fas Ligand Protein
  • Feedback, Physiological / genetics
  • Feedback, Physiological / immunology
  • Gene Expression Regulation / genetics
  • Gene Expression Regulation / immunology*
  • Genes, Regulator / genetics
  • Genes, Regulator / immunology
  • Humans
  • Membrane Glycoproteins / genetics
  • Membrane Glycoproteins / metabolism*
  • Signal Transduction / genetics
  • Stress, Physiological / genetics
  • Stress, Physiological / immunology
  • fas Receptor / metabolism*


  • Cytokines
  • FASLG protein, human
  • Fas Ligand Protein
  • Membrane Glycoproteins
  • fas Receptor