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

doi:10.1016/S0014-5793(98)01127-2

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

Fondazione IRCCS Istituto Nazionale dei Tumori

Research output: Contribution to journal › Article › peer-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 language	English
Pages (from-to)	461-465
Number of pages	5
Journal	FEBS Letters
Volume	436
Issue number	3
DOIs	https://doi.org/10.1016/S0014-5793(98)01127-2
Publication status	Published - 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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HIV/gp120 and PMA/ionomycin induced apoptosis but not activation induced cell death require PKC for Fas-L upregulation. / Accornero, Paola; Radrizzani, Marina; Carè, Alessandra; Mattia, Gianfranco; Chiodoni, Claudia; Kurrle, Roland; Colombo, Mario P.

In: FEBS Letters, Vol. 436, No. 3, 09.10.1998, p. 461-465.

Research output: Contribution to journal › Article › peer-review

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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.",

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AU - Accornero, Paola

AU - Radrizzani, Marina

AU - Carè, Alessandra

AU - Mattia, Gianfranco

AU - Chiodoni, Claudia

AU - Kurrle, Roland

AU - Colombo, Mario P.

PY - 1998/10/9

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AB - 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.

KW - Apoptosis

KW - CD4 Th1 clone

KW - Fas

KW - gp120

KW - Human immunodeficiency virus

KW - Protein kinase C

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

Abstract

Keywords

ASJC Scopus subject areas

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