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Related Experiment Videos

Fas aggregation does not correlate with Fas-mediated apoptosis.

Y Lee1, E Shacter

  • 1Laboratory of Immunology, Division of Therapeutic Proteins, Food and Drug Administration, Center for Biologics and Evaluation and Research, Bethesda, MD 20892, USA. wicknery@ninds.nih.gov

Journal of Immunology (Baltimore, Md. : 1950)
|June 22, 2001
PubMed
Summary

A serine protease inhibitor, N-tosyl-L-lysine chloromethyl ketone (TLCK), enhances Fas-mediated apoptosis in resistant cells. This enhancement is specific to Fas-induced cell death and inversely correlates with Fas aggregation.

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Fas receptor (Fas) and Fas ligand (FasL) interactions trigger apoptosis.
  • Certain cell types exhibit resistance to Fas-mediated apoptosis.
  • Fas aggregation is traditionally considered essential for apoptosis induction.

Purpose of the Study:

  • To investigate the effect of N-tosyl-L-lysine chloromethyl ketone (TLCK) on Fas-mediated apoptosis.
  • To determine the specificity of TLCK's effect on apoptotic pathways.
  • To examine the relationship between Fas aggregation and Fas-mediated apoptosis.

Main Methods:

  • Treatment of Jurkat T cells and B cell lines with TLCK.
  • Assessment of Fas-mediated apoptosis induction.
  • Analysis of TNF-alpha and TRAIL-induced apoptosis.

Related Experiment Videos

  • Evaluation of Fas expression, death-inducing signaling complex formation, and apoptosis inhibitor levels.
  • Monitoring Fas aggregation during apoptosis.

    • Main Results:

    • TLCK significantly enhanced Fas-mediated apoptosis in resistant cell lines.
    • TLCK's effect was specific to Fas-induced apoptosis, not affecting TNF-alpha or TRAIL pathways.
    • TLCK did not alter Fas expression, DISC formation, or apoptosis inhibitor levels.
    • Cells sensitized by TLCK showed reduced Fas aggregation compared to nonsensitized cells.

    Conclusions:

    • TLCK is a potent enhancer of Fas-mediated apoptosis, particularly in resistant cells.
    • The mechanism of TLCK's enhancement does not involve increased Fas expression or DISC formation.
    • Fas aggregation and Fas-mediated apoptosis are not directly correlated and may be inversely related.