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首页> 美国卫生研究院文献>Proceedings of the National Academy of Sciences of the United States of America >Repression of a matrix metalloprotease gene by E1A correlates with its ability to bind to cell type-specific transcription factor AP-2.
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Repression of a matrix metalloprotease gene by E1A correlates with its ability to bind to cell type-specific transcription factor AP-2.

机译：E1A抑制基质金属蛋白酶基因与其结合细胞类型特异性转录因子AP-2的能力有关。

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摘要

Adenovirus E1A 243-amino acid protein can repress a variety of enhancer -linked viral and cellular promoters. This repression is presumed to be mediated by its interaction with and sequestration of p3OO, a transcriptional coactivator. Type IV 72-kDa collagenase is one of the matrix metalloproteases that has been implicated in differentiation, development, angiogenesis, and tumor metastasis. We show here that the cell type-specific transcription factor AP-2 is an important transcription factor for the activation of the type IV 72-kDa collagenase promoter and that adenovirus E1A 243-amino acid protein represses this promoter by targeting AP-2. Glutathione S-transferase-affinity chromatography studies show that the E1A protein interacts with the DNA binding/dimerization region of AP-2 and that the N-terminal amino acids of E1A protein are required for this interaction. Further, E1A deletion mutants which do not bind to p3OO can repress this collagenase promoter as efficiently as the wildtype E1A protein. Because the AP-2 element is present in a variety of viral and cellular enhancers which are repressed by E1A, these studies suggest that E1A protein can repress cellular and viral promoter/enhancers by forming a complex with cellular transcription factors and that this repression mechanism may be independent of its interaction with p3OO.
机译：腺病毒E1A 243-氨基酸蛋白可以抑制多种与增强子相连的病毒和细胞启动子。推测这种抑制作用是由其与转录共激活因子p300的相互作用和螯合介导的。 IV型72 kDa胶原酶是基质金属蛋白酶之一，已与分化，发育，血管生成和肿瘤转移有关。我们在此处显示，细胞类型特异性转录因子AP-2是激活IV型72-kDa胶原酶启动子的重要转录因子，腺病毒E1A 243-氨基酸蛋白通过靶向AP-2抑制了该启动子。谷胱甘肽S-转移酶亲和层析研究表明，E1A蛋白与AP-2的DNA结合/二聚区相互作用，并且该相互作用需要E1A蛋白的N末端氨基酸。此外，不与p300结合的E1A缺失突变体可以与野生型E1A蛋白一样有效地抑制该胶原酶启动子。由于AP-2元素存在于各种被E1A抑制的病毒和细胞增强剂中，因此这些研究表明E1A蛋白可以通过与细胞转录因子形成复合物来抑制细胞和病毒启动子/增强子，并且这种抑制机制可能与其与p3OO的交互作用无关。

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