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首页> 外文期刊>Molecular and Cellular Biology >Interaction of a common factor with ATF, Sp1, or TATAA promoter elements is required for these sequences to mediate transactivation by the adenoviral oncogene E1a.
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Interaction of a common factor with ATF, Sp1, or TATAA promoter elements is required for these sequences to mediate transactivation by the adenoviral oncogene E1a.

机译：为了使这些序列介导腺病毒致癌基因E1a的反式激活，需要一个公共因子与ATF，Sp1或TATAA启动子相互作用。

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摘要

The adenovirus protein E1a stimulates transcription of both viral and cellular genes. Unlike most other transcription factors, it induces transactivation through several different promoter elements. The mechanism by which elements of diverse sequence mediate the effect of E1a is the focus of this study. Three E1a-responsive elements (an ATF site, an Sp1 site, and a TATA box containing the sequence TATAA) were studied to determine whether their interaction with a common factor is necessary for transactivation. In transfection assays, each element was used as a competitor against promoter constructs containing the other elements. The elements as competitors had no effect on basal transcription, but each competitor completely inhibited transactivation by E1a. Competitors that were not E1a responsive failed to inhibit transactivation. Therefore, either E1a itself or an E1a-inducible factor interacts with each of the elements to cause transactivation, most likely though an association with each element's specific binding protein.
机译：腺病毒蛋白E1a刺激病毒和细胞基因的转录。与大多数其他转录因子不同，它通过几种不同的启动子元件诱导反式激活。本研究的重点是各种序列的元素介导E1a效应的机制。研究了三个E1a响应元件（一个ATF位点，一个Sp1位点和一个包含序列TATAA的TATA盒），以确定它们与公共因子的相互作用对于反式激活是否必要。在转染测定中，每种元素都用作与含有其他元素的启动子构建体的竞争剂。作为竞争者的元素对基础转录没有影响，但是每个竞争者都完全抑制了E1a的反式激活。没有E1a响应的竞争对手无法抑制反式激活。因此，E1a本身或E1a诱导因子与每个元素相互作用以引起反式激活，最有可能通过与每个元素的特异性结合蛋白缔合的方式进行。

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