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Human TAF(II)135 potentiates transcriptional activation by the AF-2s of the retinoic acid, vitamin D3, and thyroid hormone receptors in mammalian cells.人转录起始因子II 135增强视黄酸、维生素D3和甲状腺激素受体的AF-2s在哺乳动物细胞中的转录激活作用。
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Endothelial cell death induced by tumor necrosis factor-alpha is inhibited by the Bcl-2 family member, A1.肿瘤坏死因子-α诱导的内皮细胞死亡受到Bcl-2家族成员A1的抑制。
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TAFII105介导核因子κB对抗凋亡基因的激活作用。

TAFII105 mediates activation of anti-apoptotic genes by NF-kappaB.

作者信息

Yamit-Hezi A, Dikstein R

机构信息

Department of Biological Chemistry, The Weizmann Institute of Science, Rehovot 76100, Israel.

出版信息

EMBO J. 1998 Sep 1;17(17):5161-9. doi: 10.1093/emboj/17.17.5161.

DOI:10.1093/emboj/17.17.5161
PMID:9724652
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1170844/
Abstract

The transcription factor NF-kappaB is important for expression of genes involved in immune responses, viral infections, cytokine signaling and stress. In addition NF-kappaB plays a crucial role in protecting cells from TNF-alpha-induced apoptotic stimuli, presumably by activating anti-apoptotic genes. Here we report that the sub-stoichiometric TFIID subunit TAFII105 is essential for activation of anti-apoptotic genes in response to TNF-alpha, serving as a transcriptional coactivator for NF-kappaB. The putative coactivator domain of TAFII105 interacts with the activation domain of the p65/RelA member of the NF-kappaB family, and further stimulates p65-induced transcription in human 293 cells. Moreover, inhibition of TAFII105 activity by overexpression of a dominant negative mutant of TAFII105 decreased NF-kappaB transcriptional activity and severely reduced cell survival in response to TNF-alpha. Similarly, expression of anti-sense TAFII105 RNA sensitized the cells to TNF-alpha cytotoxicity. These results suggest that TAFII105 is involved in activation of anti-apoptotic genes by NF-kappaB.

摘要

转录因子核因子-κB对于参与免疫反应、病毒感染、细胞因子信号传导和应激反应的基因表达至关重要。此外，核因子-κB在保护细胞免受肿瘤坏死因子-α诱导的凋亡刺激方面发挥着关键作用，这可能是通过激活抗凋亡基因来实现的。在此，我们报告亚化学计量的TFIID亚基TAFII105对于响应肿瘤坏死因子-α激活抗凋亡基因至关重要，它作为核因子-κB的转录共激活因子发挥作用。TAFII105的假定共激活结构域与核因子-κB家族的p65/RelA成员的激活结构域相互作用，并进一步刺激人293细胞中p65诱导的转录。此外，通过过表达TAFII105的显性负性突变体抑制TAFII105活性，可降低核因子-κB的转录活性，并严重降低细胞对肿瘤坏死因子-α的存活反应。同样，反义TAFII105 RNA的表达使细胞对肿瘤坏死因子-α的细胞毒性敏感。这些结果表明TAFII105参与核因子-κB对抗凋亡基因的激活。