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Focus on the splicing of Secretin GPCRs transmembrane-domain 7
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Markovic, Danijela and Grammatopoulos, Dimitris (2009) Focus on the splicing of Secretin GPCRs transmembrane-domain 7. Trends in Biochemical Sciences, Vol.34 (No.9). pp. 443-452. doi:10.1016/j.tibs.2009.06.002
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Official URL: http://dx.doi.org/10.1016/j.tibs.2009.06.002
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 signaling and, if so, what are the implications for hormonal actions and physiology?
| Item Type: | Journal Item | ||||
|---|---|---|---|---|---|
| Subjects: | Q Science > QD Chemistry | ||||
| Divisions: | Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School > Biomedical Sciences > Translational & Experimental Medicine > Metabolic and Vascular Health (- until July 2016) Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School |
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| Journal or Publication Title: | Trends in Biochemical Sciences | ||||
| Publisher: | Elsevier Science London | ||||
| ISSN: | 0968-0004 | ||||
| Official Date: | September 2009 | ||||
| Dates: |
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| Volume: | Vol.34 | ||||
| Number: | No.9 | ||||
| Number of Pages: | 10 | ||||
| Page Range: | pp. 443-452 | ||||
| DOI: | 10.1016/j.tibs.2009.06.002 | ||||
| Status: | Peer Reviewed | ||||
| Publication Status: | Published | ||||
| Access rights to Published version: | Restricted or Subscription Access |
Data sourced from Thomson Reuters' Web of Knowledge
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