关注促胰液素G蛋白偶联受体跨膜结构域7的剪接。

Focus on the splicing of secretin GPCRs transmembrane-domain 7.

作者信息

Markovic Danijela, Grammatopoulos Dimitris K

机构信息

GPCR Pathophysiology Group, Division of Endocrinology and Metabolism, Clinical Sciences Research Institute, Warwick Medical School, University of Warwick, Gibbet Hill Road, Coventry CV4 7AL, UK.

出版信息

Trends Biochem Sci. 2009 Sep;34(9):443-52. doi: 10.1016/j.tibs.2009.06.002. Epub 2009 Sep 3.

DOI:10.1016/j.tibs.2009.06.002

PMID:19733082

Abstract

The family of G-protein coupled receptors (GPCRs) is one of the largest protein families in the mammalian genome with a fundamental role in cell biology. GPCR activity is finely tuned by various transcriptional, post-transcriptional and post-translational mechanisms. Alternative pre-mRNA splicing is now emerging as a crucial process regulating GPCR biological function. Intriguingly, this mechanism appears to extensively target the Secretin family of GPCRs, especially the exon that encodes a 14 amino acid sequence that forms the distal part of 7th transmembrane helix, and exhibits an unusually high level of sequence conservation among most Secretin GPCRs. Do the "TMD7-short" receptor variants have a role as novel regulators of GPCR signallng and, if so, what are the implications for hormonal actions and physiology?

摘要

G蛋白偶联受体（GPCRs）家族是哺乳动物基因组中最大的蛋白质家族之一，在细胞生物学中具有重要作用。GPCR的活性通过各种转录、转录后和翻译后机制进行精细调节。可变前体mRNA剪接正逐渐成为调节GPCR生物学功能的关键过程。有趣的是，这种机制似乎广泛作用于GPCR的促胰液素家族，特别是编码形成第7个跨膜螺旋远端部分的14个氨基酸序列的外显子，并且在大多数促胰液素GPCR中表现出异常高的序列保守性。“TMD7-短”受体变体是否作为GPCR信号传导的新型调节因子发挥作用，如果是，对激素作用和生理学有何影响？