Linked Life Data

10900212

Source:http://linkedlifedata.com/resource/pubmed/id/10900212

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pubmed-article:10900212pubmed:abstractTextThere is great therapeutic interest in manipulating (either enhancing or suppressing) G protein-coupled receptor (GPCR) signal transduction. However, most current strategies are limited to pharmacological activation or blockade of receptors. Human gene therapy, including both overexpression and antisense approaches, may allow manipulation of GPCR signaling at steps distal to receptors. To fully understand the impact of such therapy, the transduction of signals between the multiple components of GPCR signaling and their interaction with other cellular molecules must be understood in the context of both normal physiology and disease. Defining the stoichiometric relationship among multiple components of GPCR signaling is a first step. We summarize data showing the substantial excess of G(alphas) relative to both beta-adrenergic receptors and adenylyl cyclase. A predominant idea regarding signaling via GPCRs has for over 20 years emphasized the concept of random movement and collision ("collision coupling") of proteins within the lipid bilayer of the plasma membrane. This notion does not readily account for the rapidity and fidelity of signal transduction by the multiple components involved in GPCR-G protein-effector systems, especially considering the low abundance of these proteins in cells. Recently, many components involved in signal transduction by GPCRs have been shown to exist primarily in microdomains of the plasma membrane, in particular, caveolae. These and other structures may serve to compartmentalize signals, thereby optimizing signal transduction between an agonist and specific effectors. The formation, organization, and maintenance of such structures may prove to be altered in disease states associated with disregulated signaling. In addition, we speculate that identification of genetic polymorphisms of and therapy targeted to components that are critical for determining efficacy (e.g., effectors such as adenylyl cyclase) will provide important future therapeutic strategies.lld:pubmed
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pubmed-article:10900212pubmed:pagination407-12lld:pubmed
pubmed-article:10900212pubmed:dateRevised2009-11-19lld:pubmed
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pubmed-article:10900212pubmed:articleTitleStoichiometry and compartmentation in G protein-coupled receptor signaling: implications for therapeutic interventions involving G(s).lld:pubmed
pubmed-article:10900212pubmed:affiliationDepartment of Pharmacology, School of Medicine, University of California, San Diego, La Jolla 92093-0636, USA.lld:pubmed
pubmed-article:10900212pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:10900212pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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