...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cell biology international. >Vps26B-retromer negatively regulates plasma membrane resensitization of PAR-2
【24h】

Vps26B-retromer negatively regulates plasma membrane resensitization of PAR-2

机译：Vps26B-retromer负调节PAR-2的质膜再敏化

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Retromer is a trimeric complex composed of Vps26, Vps29, and Vps35 and has been shown to be involved in trafficking and sorting of transmembrane proteins within the endosome. The Vps26 paralog, Vps26B, defines a distinct retromer complex (Vps26B-retromer) in vivo and in vitro. Although endosomally associated, Vps26B-retromer does not bind the established retromer transmembrane cargo protein, cation-independent mannose 6-phosphate receptor (CI-M6PR), indicating it has a distinct role to retromer containing the Vps26A paralog. In the present study we use the previously established Vps26B-expressing HEK293 cell model to address the role of Vps26B-retromer in trafficking of the protease activated G-protein coupled receptor PAR-2 to the plasma membrane. In these cells there is no apparent defect in the initial activation of the receptor, as evidenced by release of intracellular calcium, ERK1/2 signaling and endocytosis of activated receptor PAR-2 into degradative organelles. However, we observe a significant delay in plasma membrane repopulation of the protease activated G protein-coupled receptor PAR-2 following stimulation, resulting in a defect in PAR-2 activation after resensitization. Here we propose that PAR-2 plasma membrane repopulation is regulated by Vps26B-retromer, describing a potential novel role for this complex.
机译：Retromer是由Vps26，Vps29和Vps35组成的三聚体复合物，已被证明与内体中跨膜蛋白的运输和分选有关。 Vps26旁系同源物Vps26B在体内和体外定义了独特的逆转录复合物（Vps26B-retromer）。尽管是内体相关的，Vps26B-retromer并不结合已建立的逆转录子跨膜货物蛋白，即不依赖阳离子的甘露糖6-磷酸受体（CI-M6PR），表明它对包含Vps26A旁系同源物的逆转录子具有独特的作用。在本研究中，我们使用先前建立的表达Vps26B的HEK293细胞模型来解决Vps26B-retromer在将蛋白酶激活的G蛋白偶联受体PAR-2转运到质膜中的作用。在这些细胞中，受体的初始活化没有明显的缺陷，如细胞内钙的释放，ERK1 / 2信号传导和活化的受体PAR-2向降解细胞器的内吞作用所证明的。但是，我们观察到刺激后，蛋白酶激活的G蛋白偶联受体PAR-2的质膜重新聚集显着延迟，导致再敏化后PAR-2激活存在缺陷。在这里，我们提出PAR-2质膜的重新分布受Vps26B-retromer的调节，描述了该复合物的潜在新作用。

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