...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cellular Physiology and Biochemistry >Ubiquitin-Specific Peptidase USP22 Negatively Regulates the STAT Signaling Pathway by Deubiquitinating SIRT1
【24h】

Ubiquitin-Specific Peptidase USP22 Negatively Regulates the STAT Signaling Pathway by Deubiquitinating SIRT1

机译：泛素特异性肽酶USP22通过去泛素化SIRT1负调控STAT信号通路。

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

摘要

Background/Aims: The ubiquitin-specific peptidase USP22 mediates various cellular and organismal processes, such as cell growth, apoptosis, and tumor malignancy. However, the molecular mechanisms that regulate USP22 activity remain poorly understood. Here we identify STAT3 as a new USP22 interactor. Methods:· We used western blotting and RT-PCR to measure key protein, acetylated STAT3, and mRNA levels in HEK293 and colorectal cancer cell lines transfected with expression plasmids or specific siRNAs. Co-immunoprecipitation was used to demonstrate protein-protein interaction and protein complex composition. Results: USP22 overexpression down-regulated STAT3 acetylation by deubiquitinating SIRT1. The three proteins were found to be present in a single protein complex. SiRNA-mediated depletion of endogenous USP22 resulted in SIRT1 destabilization and elevated STAT3 acetylation. Consistent with this finding, USP22 also down-regulated the expression of two known STAT3 target genes, MMP9 and TWIST. Conclusion: We show that USP22 is a new regulator of the SIRT1-STAT3 signaling pathway and report a new mechanistic explanation for cross talk between USP22 and the SIRT1-STAT pathways.
机译：背景/目的：泛素特异性肽酶USP22介导各种细胞和生物过程，例如细胞生长，凋亡和肿瘤恶性肿瘤。但是，调节USP22活性的分子机制仍然知之甚少。在这里，我们将STAT3识别为新的USP22相互作用子。方法：·我们使用Western印迹和RT-PCR测量了用表达质粒或特异性siRNA转染的HEK293和结直肠癌细胞系中的关键蛋白，乙酰化STAT3和mRNA水平。共免疫沉淀被用来证明蛋白质-蛋白质相互作用和蛋白质复合物组成。结果：USP22过表达通过去泛素化SIRT1下调STAT3乙酰化。发现这三种蛋白质存在于单一蛋白质复合物中。 SiRNA介导的内源性USP22耗竭导致SIRT1不稳定和STAT3乙酰化升高。与该发现一致的是，USP22还下调了两个已知的STAT3靶基因MMP9和TWIST的表达。结论：我们表明，USP22是SIRT1-STAT3信号通路的新调节剂，并报告了USP22与SIRT1-STAT通路之间串扰的新机理解释。

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