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首页> 外文期刊>Molecular cell >Exon identity established through differential antagonism between exonic splicing silencer-bound hnRNP A1 and enhancer-bound SR proteins.
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Exon identity established through differential antagonism between exonic splicing silencer-bound hnRNP A1 and enhancer-bound SR proteins.

机译：外显子同一性通过外显子剪接沉默子结合的hnRNP A1和增强子结合的SR蛋白之间的拮抗作用建立。

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摘要

SR proteins recognize exonic splicing enhancer (ESE) elements and promote exon use, whereas certain hnRNP proteins bind to exonic splicing silencer (ESS) elements and block exon recognition. We investigated how ESS3 in HIV-1 tat exon 3 blocks splicing promoted by one SR protein (SC35) but not another (SF2/ASF). hnRNP A1 mediates silencing by binding initially to a required high-affinity site in ESS3, which then promotes further hnRNP A1 association with the upstream region of the exon. Both SC35 and SF2/ASF recognize upstream ESE motifs, but only SF2/ASF prevents secondary hnRNP A1 binding, presumably by blocking its cooperative propagation along the exon. The differential antagonism between a negative and two positive regulators exemplifies how inclusion of an alternative exon can be modulated.
机译：SR蛋白识别外显子剪接增强子（ESE）元素并促进外显子的使用，而某些hnRNP蛋白与外显子剪接沉默子（ESS）元素结合并阻止外显子的识别。我们调查了HIV-1 tat外显子3中的ESS3如何阻止一种SR蛋白（SC35）促进另一种（SF2 / ASF）刺激的剪接。 hnRNP A1通过首先绑定到ESS3中所需的高亲和力位点来介导沉默，然后进一步促进hnRNP A1与外显子的上游区域进一步缔合。 SC35和SF2 / ASF都识别上游ESE基序，但是只有SF2 / ASF阻止了hnRNP A1的二级结合，大概是通过阻止其沿外显子的协同传播来实现的。负调节剂和两个正调节剂之间的差异拮抗作用举例说明了如何调节其他外显子的包含。

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