Cardiff University | Prifysgol Caerdydd ORCA
Online Research @ Cardiff 
WelshClear Cookie - decide language by browser settings

Regulation of cellular signal transduction pathways by the extracellular calcium-sensing receptor

Brennan, Sarah C. ORCID: https://orcid.org/0000-0002-8719-4367 and Conigrave, Arthur 2009. Regulation of cellular signal transduction pathways by the extracellular calcium-sensing receptor. Current Pharmaceutical Biotechnology 10 (3) , pp. 270-281. 10.2174/138920109787847484

Full text not available from this repository.

Abstract

The extracellular calcium-sensing receptor (CaR) is a class III G-protein coupled receptor that coordinates cellular responses to changes in extracellular free Ca2+ or amino acid concentrations as well as ionic strength and pH. It regulates signalling cascades via recruiting and controlling the activities of various heterotrimeric G-proteins, including Gq/11, Gi/0, and G12/13, even Gs in some “unusual” circumstances, thereby inducing changes in the metabolism of membrane lipids, the phosphorylation state of protein kinases and their targets, the activation state of monomeric G-proteins and the levels of intracellular second messengers including cAMP, Ca2+ ions, fatty acids and other small molecules. According to its site(s) of expression and available signalling pathways, the CaR modulates cell proliferation and survival, differentiation, peptide hormone secretion, ion and water transport and various other processes. In this article we consider the complex intracellular mechanisms by which the CaR elicits its cellular functions. We also consider some of the better understood CaR-regulated cell functions and the nature of the signalling mechanisms that support them.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Biosciences
ISSN: 1389-2010
Last Modified: 27 Oct 2022 09:26
URI: https://orca.cardiff.ac.uk/id/eprint/65842

Citation Data

Cited 46 times in Scopus. View in Scopus. Powered By Scopus® Data

Actions (repository staff only)

Edit Item Edit Item