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

被引：11

作者：

Accornero, P

Radrizzani, M

Carè, A

Mattia, G

Chiodoni, C

Kurrle, R

Colombo, MP

机构：

[1] Ist Nazl Tumori, Div Expt Oncol D, I-20133 Milan, Italy

[2] Ist Super Sanita, I-00161 Rome, Italy

[3] Behringwerke AG, D-3550 Marburg, Germany

来源：

FEBS LETTERS | 1998年 / 436卷 / 03期

关键词：

human immunodeficiency virus; gp120; apoptosis; protein kinase C; Fas; CD4(+) th1 clone;

D O I：

10.1016/S0014-5793(98)01127-2

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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 Fast, 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, (C) 1998 Federation of European Biochemical Societies.

引用

收藏

页码：461 / 465

页数：5

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