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野生型而非突变型p53可通过干扰基础转录因子与TATA基序的结合在体外抑制转录起始。

Wild-type but not mutant p53 can repress transcription initiation in vitro by interfering with the binding of basal transcription factors to the TATA motif.

作者信息

Ragimov N, Krauskopf A, Navot N, Rotter V, Oren M, Aloni Y

机构信息

Department of Molecular Genetics and Virology, Weizmann Institute of Science, Rehovot, Israel.

出版信息

Oncogene. 1993 May;8(5):1183-93.

PMID:8479742
Abstract

It has previously been shown that excess wild type (wt) p53 can repress the transcriptional activity of a variety of promoters in intact cells. To determine whether this transcriptional repression represented a direct effect of p53, wt and mutant p53 were prepared from E. coli-produced p53 and from insect cells infected with a recombinant baculovirus. When added into an in vitro transcription system, wt p53, but not mutant p53 reduced markedly transcription from the c-myc promoter, as well as from an array of other promoters, with the exception of an MHC class I gene promoter. The presence of wt p53 seemed to affect specifically the formation of the transcription preinitiation complex because preformed initiation complexes were completely refractory to wt p53, as was also the process of transcript elongation. Wild-type but not mutant p53 interfered with the stable binding of TBP and TFIIA to the TATA motif, although both wt and mutant p53 could associate in vitro with purified TBP. We propose that upon binding to TBP, wt but not mutant p53 specifically blocks the ability of TBP to engage in interactions required for efficient transcriptional initiation. This may account, at least in part, for the ability of excess wt p53 to inhibit cell proliferation and to interfere with neoplastic processes.

摘要

先前已经表明,过量的野生型(wt)p53可以抑制完整细胞中多种启动子的转录活性。为了确定这种转录抑制是否代表p53的直接作用,从大肠杆菌产生的p53和感染重组杆状病毒的昆虫细胞中制备了wt和突变型p53。当添加到体外转录系统中时,wt p53而非突变型p53显著降低了c-myc启动子以及一系列其他启动子的转录,但MHC I类基因启动子除外。wt p53的存在似乎特异性地影响转录起始前复合物的形成,因为预先形成的起始复合物对wt p53完全不敏感,转录延伸过程也是如此。野生型而非突变型p53干扰了TBP和TFIIA与TATA基序的稳定结合,尽管wt和突变型p53在体外都可以与纯化的TBP结合。我们提出,与TBP结合后,wt而非突变型p53特异性地阻断了TBP参与有效转录起始所需相互作用的能力。这可能至少部分解释了过量wt p53抑制细胞增殖和干扰肿瘤发生过程的能力。

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