Class A and B GPCRs trigger rapid Gα(s) translocation to late and slow recycling endosomes

A类和B类GPCR触发Gα(s)快速易位至晚期和慢速循环内体。

阅读:2

Abstract

Gα(s) is classically known for mediating G protein-coupled receptor (GPCR) signaling at the plasma membrane (PM), but it is now established that Gα(s) also supports a second wave of signaling from internalized GPCRs within early endosomes. However, the mechanisms underlying Gα(s) trafficking remain unclear. Here, using live-cell confocal microscopy and bioluminescence resonance energy transfer (BRET) assays, we investigated Gα(s)-GFP dynamics following activation of class A (β(2)AR) and class B (V(2)R) receptors, which exhibit different level of endosomal signaling. Our findings demonstrate that Gα(s) rapidly ( < 2 min) translocates to late (Rab7) and slow recycling (Rab11) endosomes, bypassing the classical endocytic route and displaying only transient colocalization with receptors. This trafficking depends on Gα(s) activation at the PM, its release from the membrane, and an intact palmitoylation site, but occurs independently of receptor internalization. This work shed light on non-canonical route for Gα(s) endosomal trafficking, with important implications for endosomal GPCR signaling.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。