HIV-1反式激活因子在人单核细胞中触发的诱导肿瘤坏死因子-α的信号通路。
Signaling pathways triggered by HIV-1 Tat in human monocytes to induce TNF-alpha.
作者信息
Bennasser Yamina, Badou Abdallah, Tkaczuk Jean, Bahraoui Elmostafa
机构信息
Laboratoire d'Immuno-Virologie, EA 3038, Université Paul Sabatier 118, route de Narbonne, 31062, Toulouse Cedex, France.
出版信息
Virology. 2002 Nov 10;303(1):174-80. doi: 10.1006/viro.2002.1676.
In this study we investigated the signaling pathways triggered by Tat in human monocyte to induce TNF-alpha. In monocytes, the calcium, the PKA, and the PKC pathways are highly implicated in the expression of cytokine genes. Thus, these three major signaling pathways were investigated. Our data show that (i) PKC and calcium pathways are required for TNF-alpha production, whereas the PKA pathway seems to be not involved; (ii) downstream from PKC, activation of NFkappaB is essential while ERK1/2 MAP kinases, even though activated by Tat, are not directly involved in the pathway signaling leading to TNF-alpha production.
在本研究中，我们调查了Tat在人单核细胞中触发以诱导肿瘤坏死因子-α（TNF-α）的信号通路。在单核细胞中，钙、蛋白激酶A（PKA）和蛋白激酶C（PKC）通路与细胞因子基因的表达高度相关。因此，对这三条主要信号通路进行了研究。我们的数据表明：（i）PKC和钙通路是产生TNF-α所必需的，而PKA通路似乎未参与其中；（ii）在PKC的下游，核因子κB（NFκB）的激活至关重要，而细胞外信号调节激酶1/2（ERK1/2）丝裂原活化蛋白激酶虽然被Tat激活，但并不直接参与导致TNF-α产生的信号通路。
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