...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Molecular and Cellular Biology >Serum response factor and protein-mediated DNA bending contribute to transcription of the dystrophin muscle-specific promoter.
【24h】

Serum response factor and protein-mediated DNA bending contribute to transcription of the dystrophin muscle-specific promoter.

机译：血清反应因子和蛋白质介导的DNA弯曲有助于肌营养不良蛋白肌肉特异性启动子的转录。

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The minimal muscle-specific dystrophin promoter contains the consensus sequence CC(A/T)6GG, or the CArG element, which can be found in serum-inducible or muscle-specific promoters. The serum response factor (SRF), which mediates the transcriptional activation of the c-fos gene in response to serum stimulation, can bind to different CArG box elements, suggesting that it could be involved in muscle-constitutive transcription. Here we show that SRF binds to the dystrophin promoter and regulates its muscle-specific transcription. In transient transfections, an altered-binding-specificity SRF mutant restores the muscle-constitutive transcription of a dystrophin promoter with a mutation in its CArG box element. The muscle-constitutive transcription of the dystrophin promoter also requires the sequence GAAACC immediately downstream of the CArG box. This sequence is recognized by a novel DNA bending factor which was named dystrophin promoter-bending factor (DPBF). Mutations of the CArG flanking sequence abolish both DPBF binding and the promoter activity in muscle cells. Its replacement with a p62/ternary complex factor binding site changes the promoter specificity from muscle constitutive to serum responsive. These results show that, on the dystrophin promoter, the transcriptional activation induced by SRF requires the DNA bending induced by DPBF. The bending, next to the CArG box, could promote interactions between SRF and other proteins in the transcriptional complex.
机译：最小的肌肉特异性肌营养不良蛋白启动子包含共有序列CC（A / T）6GG或CArG元素，可以在血清诱导型或肌肉特异性启动子中找到。血清应答因子（SRF）介导c-fos基因的转录激活以响应血清刺激，可与不同的CArG box元件结合，表明它可能参与了肌肉组成型转录。在这里，我们显示SRF与肌营养不良蛋白启动子结合并调节其肌肉特异性转录。在瞬时转染中，结合特异性改变的SRF突变体恢复了肌营养不良蛋白启动子的肌肉组成转录，其CArG盒元件中存在突变。肌营养不良蛋白启动子的肌肉组成型转录也需要在CArG盒下游紧接的序列GAAACC。该序列被称为抗肌萎缩蛋白启动子弯曲因子（DPBF）的新型DNA弯曲因子所识别。 CArG侧翼序列的突变消除了DPBF结合和肌肉细胞中的启动子活性。用p62 /三元复合因子结合位点替代其可将启动子特异性从肌肉组成性改变为血清反应性。这些结果表明，在肌营养不良蛋白启动子上，SRF诱导的转录激活需要DPBF诱导的DNA弯曲。 CArG框旁边的弯曲可能会促进SRF与转录复合物中其他蛋白质之间的相互作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号