Linked Life Data

18001849

Source:http://linkedlifedata.com/resource/pubmed/id/18001849

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2007-12-6
pubmed:abstractText
A large body of evidence indicates that agonists of some G protein-coupled receptors (GPCRs) can activate growth factor receptor tyrosine kinases (RTKs) in the absence of added growth factor. This phenomenon, called transactivation, is an important pathway that contributes to growth-promoting activity of many GPCR ligands. Reciprocally, recent advances indicate that RTKs utilize GPCR signalling molecules to transduce signals and that RTK ligands themselves can transactivate GPCRs. This novel transactivation process, which places GPCR signalling downstream of RTKs, either requires the production of a GPCR ligand of the transactivated GPCR or occurs in a ligand independent manner within an integrated signalling network. Here, we provide an overview of the molecular mechanisms involved in this novel cross-communication between GPCRs and RTKs and discuss its relevance in the specification of growth factor signalling and functions.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0165-6147
pubmed:author
pubmed:issnType
Print
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
602-7
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
GPCR-jacking: from a new route in RTK signalling to a new concept in GPCR activation.
pubmed:affiliation
Institut de Génomique Fonctionnelle, Universités de Montpellier, CNRS UMR 5203, 141 rue de la Cardonille, Montpellier CEDEX 5, F-34094, France.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't