HIV-1 Nef interacts with inositol trisphosphate receptor to activate calcium signaling in T cells.
HIV-1 Nef interacts with inositol trisphosphate receptor to activate calcium signaling in T cells.
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DOI：
10.1084/jem.20012039
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发表时间：
2002-04-15
期刊：
影响因子：
--
通讯作者：
Saksela K
中科院分区：
文献类型：
--
作者：
Manninen A;Saksela K
HIV-1 pathogenicity factor Nef has been shown to modulate calcium signaling in host cells, but the underlying molecular mechanisms have remained unclear. Here we show that calcium/calcineurin-dependent activation of nuclear factor of activated T cells (NFAT) by Nef in Jurkat T cells requires the endoplasmic reticulum-resident inositol trisphosphate receptor (IP3R), but yet does not involve increase in phospholipase-Cγ1 (PLCγ1)-catalyzed production of IP3 or depletion of IP3-regulated intracellular calcium stores. Nef could be coprecipitated with endogenous IP3R type-1 (IP3R1) from Nef-transfected Jurkat T cells as well as from HIV-infected primary human peripheral mononuclear cells. Thus, the Nef/IP3R1-interaction defines a novel T cell receptor–independent mechanism by which Nef can promote T cell activation, and appears to involve atypical IP3R-triggered activation of plasma membrane calcium influx channels in a manner that is uncoupled from depletion of intracellular calcium stores.
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