Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2006-7-24
pubmed:abstractText
Regulators of G protein signaling (RGS proteins) bind directly to activated Galpha subunits to inhibit their signaling. However, recent findings show that RGS proteins selectively regulate signaling by certain G protein-coupled receptors (GPCRs) in cells, irrespective of the coupled G protein. New studies support an emerging model that suggests RGS proteins utilize both direct and indirect mechanisms to form stable functional pairs with preferred GPCRs to selectively modulate the signaling functions of those receptors and linked G proteins. Here, we discuss these findings and their implications for established models of GPCR signaling.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1084-9521
pubmed:author
pubmed:issnType
Print
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
383-9
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Cellular mechanisms that determine selective RGS protein regulation of G protein-coupled receptor signaling.
pubmed:affiliation
Department of Pharmacology, Emory University School of Medicine, G205 Rollins Research Center, 1510 Clifton Road, Atlanta, GA 30322, USA.
pubmed:publicationType
Journal Article, Review, Research Support, N.I.H., Extramural