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首页> 外文期刊>Molecular and Cellular Biology >Reversal of in vitro p53 squelching by both TFIIB and TFIID.
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Reversal of in vitro p53 squelching by both TFIIB and TFIID.

机译：TFIIB和TFIID均可逆转体外p53抑制。

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p53, the protein encoded by one of the most significant human tumor suppressor genes, is a sequence-specific transcriptional activator. When activated by a double-stranded DNA break, p53 function arrests cells in G1 and can induce apoptosis. Transcriptional activation function is critical for p53 tumor suppression, although transcriptional repressing and nontranscriptional functions of p53 may contribute. p53 activation requires that it bind to TFIID through interactions with TATA box-binding protein (TBP)-associated factors and potentially with TBP. Here, we studied the mechanism of p53 activation using in vitro transcription and a sufficiently high p53 concentration to squelch activated transcription. Squelching is thought to result when target molecules that interact with activation domains are titrated by binding to excess activator. Addition of either excess TFIIB or TFIID but not other proteins required for p53-activated transcription reversed squelching by high p53 concentrations, whereas neither stimulated transcription in reactions without excess p53. These results reveal that both TFIIB and TFIID are inhibited by high concentrations of p53 and suggest that p53 activation may work through direct or indirect interactions with both TFIIB and TFIID.
机译：p53是一种由人类最重要的人类抑癌基因编码的蛋白质，是一种序列特异性转录激活因子。当被双链DNA断裂激活时，p53功能会阻滞G1细胞并诱导凋亡。转录激活功能对p53肿瘤抑制至关重要，尽管p53的转录抑制和非转录功能可能有所贡献。 p53激活要求它通过与TATA盒结合蛋白（TBP）相关因子以及可能与TBP的相互作用与TFIID结合。在这里，我们研究了使用体外转录和足够高的p53浓度抑制静默激活转录的p53激活机制。当与活化域相互作用的靶分子通过与过量的活化剂结合而被滴定时，认为会导致静噪。添加过量的TFIIB或TFIID，但不添加p53激活的转录所需的其他蛋白质，则可以通过高p53浓度逆转静噪，而在没有过量p53的反应中，都不能刺激转录。这些结果表明高浓度的p53抑制了TFIIB和TFIID，并且表明p53激活可能通过与TFIIB和TFIID的直接或间接相互作用起作用。

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