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首页> 外文期刊>Journal of Cellular Physiology >Inhibition of ShcA isoforms p46/p52Shc enhances HIV-1 replication in CD4+ T-lymphocytes.
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Inhibition of ShcA isoforms p46/p52Shc enhances HIV-1 replication in CD4+ T-lymphocytes.

机译：抑制ShcA亚型p46 / p52Shc增强hiv - 1在CD4 + t淋巴球复制。

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摘要

HIV-1 infection decreases the number of CD4(+) T-cells, and apoptosis has been suggested among the mechanisms. Proteins of the Shc family are involved in a complex network of signal transduction, differentiation, and apoptotic response to stress in many different cell types. Out of three homologous gene products (ShcA, ShcB, and ShcC), only two splicing variants of ShA are expressed in T-lymphocytes, namely p46Shc and p52Shc. In the present study, we report that inhibition of p46Shc and p52Shc by a dominant negative mutant enhances the yield of HIV-1 particles production without affecting efficiency of viral gene expression in CD4(+)-infected cells. The increase in HIV-1 replication in cells expressing the dominant negative mutant isoform ultimately correlates with a decrease in the percentage of cells entering apoptosis. The data presented suggest that ShcA proteins can play a role in committing CD4(+) T-cells to apoptosis, as a response to HIV-1 infection.
机译：hiv - 1感染的CD4(+)的数量减少t细胞和细胞凋亡被建议的机制。参与复杂的信号网络转导、分化和凋亡对压力的反应在许多不同的细胞类型。三个同源基因产物(ShcA,ShcB和ShcC),只有两个剪接变体在t淋巴球沙表示,即p46Shc和p52Shc。抑制p46Shc和p52Shc占主导地位负突变提高hiv - 1的产量粒子在不影响生产效率病毒基因表达的CD4(+)来华细胞。表达的主要负突变同种型最终与减少进入细胞凋亡细胞的比例。提出了建议ShcA蛋白质可以发挥在提交CD4 (+) t细胞凋亡,作为应对hiv - 1感染。

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