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Related Experiment Videos

Vav regulates peptide-specific apoptosis in thymocytes

Y Y Kong1, K D Fischer, M F Bachmann

  • 1Amgen Institute, University of Toronto, Toronto, Ontario, Canada M5G 2C1.

The Journal of Experimental Medicine
|December 8, 1998
PubMed
Summary

The protooncogene Vav is crucial for T cell apoptosis. Its absence prevents T cell death by regulating actin cytoskeleton and protein kinase C (PKC) signaling.

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • The protooncogene Vav acts as a GDP/GTP exchange factor (GEF) for Rho-like small GTPases.
  • Vav plays a role in cytoskeletal reorganization and cytokine production in T cells.

Purpose of the Study:

  • To investigate the role of Vav in T cell antigen receptor (TCR) mediated thymocyte apoptosis.
  • To elucidate the molecular mechanisms by which Vav regulates TCR-induced cell death.

Main Methods:

  • Utilized gene-targeted mice lacking Vav (vav-/-).
  • Assessed thymocyte selection, apoptosis, calcium mobilization, and actin polymerization.
  • Investigated the involvement of protein kinase C (PKC) and cytochalasin D.

Main Results:

Related Experiment Videos

  • Vav-deficient thymocytes exhibit defects in positive and negative selection and are resistant to apoptosis.
  • Vav acts upstream of mitochondrial pore opening and caspase activation.
  • Vav regulates peptide-specific calcium mobilization and actin polymerization, pathways involving PKC-theta.

Conclusions:

  • Peptide-triggered thymocyte apoptosis is mediated by Vav activation.
  • Vav signaling involves actin cytoskeleton remodeling and subsequent activation of a PKC isoform.
  • Vav is a key regulator of T cell development and apoptosis.