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TATA Binding Protein Discriminates between Different Lesions on DNA, Resulting in a Transcription Decrease

机译:TATA结合蛋白可区分DNA上的不同病变,从而导致转录降低

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DNA damage recognition by basal transcription factors follows different mechanisms. Using transcription-competition, nitrocellulose filter binding, and DNase I footprinting assays, we show that, although the general transcription factor TFIIH is able to target any kind of lesion which can be repaired by the nucleotide excision repair pathway, TATA binding protein (TBP)-TFIID is more selective in damage recognition. Only genotoxic agents which are able to induce kinked DNA structures similar to the one for the TATA box in its TBP complex are recognized. Indeed, DNase I footprinting patterns reveal that TBP protects equally 4 nucleotides upstream and 6 nucleotides downstream from the A-T (at position ?29 of the noncoding strand) of the adenovirus major late promoter and from the G-G of a cisplatin-induced 1,2-d(GpG) cross-link. Together, our results may partially explain differences in transcription inhibition rates following DNA damage.
机译:基础转录因子对DNA损伤的识别遵循不同的机制。使用转录竞争,硝酸纤维素滤膜结合和DNase I足迹测定法,我们显示,尽管一般转录因子TFIIH能够靶向可通过核苷酸切除修复途径修复的任何类型的病变,但TATA结合蛋白(TBP) -TFIID在损坏识别方面更具选择性。仅识别能够诱导类似于其TBP复合物中TATA盒的扭结DNA结构的遗传毒性剂。确实,DNase I足迹模式显示,TBP在腺病毒主要晚期启动子的AT(非编码链的第29位)和顺铂诱导的1,2- GG的保护上均具有上游4个核苷酸和下游6个核苷酸的保护。 d(GpG)交叉链接。在一起,我们的结果可能部分解释了DNA损伤后转录抑制率的差异。

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