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Related Experiment Videos

TCR pathway involves ICBP90 gene down-regulation via E2F binding sites.

Abdul-Qader Abbady1, Christian Bronner, Kawtar Bathami

  • 1INSERM UMR-S 392, and Laboratoire de Physiopathologie Cellulaire & Moléculaire et Infection, Institut de Parasitolgie et de Pathologie Tropicale, Faculté de Médecine, 3 rue Koeberlé, 67000 Strasbourg, France.

Biochemical Pharmacology
|June 21, 2005
PubMed
Summary

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T-cell receptor (TCR) activation down-regulates ICBP90 expression, leading to cell growth arrest. This ICBP90 decrease is crucial for G1 arrest preceding T-lymphocyte cell death.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Cycle Regulation

Background:

  • Antigen-induced T-lymphocyte cell death is vital for immune function.
  • T-cell receptor (TCR) signaling regulates T-cell homeostasis.
  • ICBP90 is essential for the G1/S cell cycle transition.

Purpose of the Study:

  • To investigate the regulation of ICBP90 by the TCR pathway in Jurkat T-cells.
  • To elucidate the role of ICBP90 in TCR-induced T-cell cycle arrest and apoptosis.

Main Methods:

  • TCR triggering in Jurkat cells.
  • Analysis of ICBP90, cyclin D3, and topoisomerase IIalpha expression.
  • Stimulation with PMA and calcium ionophore.
  • Luciferase reporter assay for gene promoter activity.

Related Experiment Videos

  • Site-directed mutagenesis of E2F binding sites in the ICBP90 promoter.

    • Main Results:

    • TCR triggering decreased ICBP90, cyclin D3, and topoisomerase IIalpha expression.
    • PMA and/or A23187 stimulation down-regulated ICBP90.
    • Decreased ICBP90 correlated with cell growth arrest.
    • TCR pathway activation inhibited ICBP90 gene promoter activity.
    • E2F-a and E2F-c binding sites mediate TCR-induced ICBP90 down-regulation.

    Conclusions:

    • TCR signaling regulates ICBP90 gene expression via the pRb/E2F complex.
    • Down-regulation of ICBP90 is a key event in G1 arrest preceding T-cell death.