HIV/gp120 and PMA/ionomycin induced apoptosis but not activation induced cell death require PKC for Fas-L upregulation

Paola Accornero, Marina Radrizzani, Alessandra Carè, Gianfranco Mattia, Claudia Chiodoni, Roland Kurrle, Mario P. Colombo

Research output: Contribution to journalArticlepeer-review

Abstract

HIV protein gp120 in combination with T cell antigen receptor (TCR) triggering induces apoptosis (gp120-apoptosis) in Th1 cells. Gp120-apoptosis occurs by induction of Fas-L and subsequent triggering of the Fas apoptotic pathway. Here, through the use of several compounds inhibiting induction of Fas-L, we show that, in a Th1 clone, a protein kinase C (PKC) independent pathway activated by TCR stimulation is distinguishible from a PKC dependent pathway activated by either phorbol 12-myristate 13-acetate (PMA)/ionomycin or asynchronous stimulation of TCR and CD4 as occurs in gp120-apoptosis. Copyright (C) 1998 Federation of European Biochemical Societies.

Original languageEnglish
Pages (from-to)461-465
Number of pages5
JournalFEBS Letters
Volume436
Issue number3
DOIs
Publication statusPublished - Oct 9 1998

Keywords

  • Apoptosis
  • CD4 Th1 clone
  • Fas
  • gp120
  • Human immunodeficiency virus
  • Protein kinase C

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

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