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Signaling and transcriptional control of Fas ligand gene expression

M M Kavurma1, L M Khachigian

  • 1Centre for Thrombosis and Vascular Research, Department of Pathology, The University of New South Wales, Sydney, Australia.

Cell Death and Differentiation
|March 26, 2003
PubMed

Insights

Fas ligand (FasL) triggers apoptosis by activating caspases. Nuclear factors regulate FasL gene expression transcriptionally, impacting cellular degradation and death, particularly in diseases like atherosclerosis.

Area of Science:

  • Molecular Biology
  • Immunology
  • Cellular Biology

Background:

  • Fas ligand (FasL), a tumor necrosis factor family member, initiates apoptosis through Fas receptor binding.
  • Apoptosis involves sequential caspase activation, mitochondrial cytochrome c release, and cellular degradation.
  • Understanding FasL's role is crucial in diseases involving programmed cell death.

Purpose of the Study:

  • To review recent advances in understanding the molecular mechanisms controlling FasL gene expression.
  • To elucidate the transcriptional regulation of FasL.
  • To highlight the role of nuclear factors in FasL expression.

Main Methods:

  • Review of existing literature on FasL gene expression and regulation.
  • Analysis of studies identifying nuclear factors involved in FasL transcription.
  • Examination of the coexpression of FasL and regulatory factors in pathophysiological settings.

Main Results:

  • Multiple nuclear factors, including NFAT, NF-κB, Sp1, EGR, IRF, c-Myc, and FOX, activate FasL expression.
  • These factors can act alone or cooperatively to modulate FasL transcription.
  • Coexpression of these factors with FasL is observed in disease states such as human atherosclerotic lesions.

Conclusions:

  • FasL gene expression is tightly controlled at the transcriptional level by a network of nuclear factors.
  • These regulatory mechanisms are relevant to pathophysiological conditions, including atherosclerosis.
  • Further research into these signaling and transcriptional pathways is warranted.

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