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dc.contributor.author Rajagopal, K
dc.contributor.author Lefkowitz, RJ
dc.contributor.author Rockman, HA
dc.coverage.spatial United States
dc.date.accessioned 2012-10-24T18:35:24Z
dc.date.issued 2005-11
dc.identifier http://www.ncbi.nlm.nih.gov/pubmed/16276410
dc.identifier.citation J Clin Invest, 2005, 115 (11), pp. 2971 - 2974
dc.identifier.issn 0021-9738
dc.identifier.uri http://hdl.handle.net/10161/5931
dc.description.abstract Classically, 7 transmembrane receptors transduce extracellular signals by coupling to heterotrimeric G proteins, although recent in vitro studies have clearly demonstrated that they can also signal via G protein-independent mechanisms. However, the physiologic consequences of this unconventional signaling, particularly in vivo, have not been explored. In this issue of the JCI, Zhai et al. demonstrate in vivo effects of G protein-independent signaling by the angiotensin II type 1 receptor (AT1R) (see the related article beginning on page 3045). In studies of the mouse heart, they compare the physiologic and biochemical consequences of transgenic cardiac-specific overexpression of a mutant AT1R incapable of G protein coupling with those of a wild-type receptor. Their results not only provide the first glimpse of the physiologic effects of this newly appreciated mode of signaling but also provide important and previously unappreciated clues as to the underlying molecular mechanisms.
dc.format.extent 2971 - 2974
dc.language eng
dc.relation.ispartof J Clin Invest
dc.relation.isversionof 10.1172/JCI26950
dc.subject Animals
dc.subject Mice
dc.subject Receptor, Angiotensin, Type 1
dc.subject Receptors, G-Protein-Coupled
dc.subject Signal Transduction
dc.title When 7 transmembrane receptors are not G protein-coupled receptors.
dc.type Journal Article
duke.description.endpage 2974 en_US
duke.description.issue 11 en_US
duke.description.startpage 2971 en_US
duke.description.volume 115 en_US
dc.relation.journal Journal of Clinical Investigation en_US
pubs.author-url http://www.ncbi.nlm.nih.gov/pubmed/16276410
pubs.issue 11
pubs.organisational-group /Duke
pubs.organisational-group /Duke/School of Medicine
pubs.organisational-group /Duke/School of Medicine/Basic Science Departments
pubs.organisational-group /Duke/School of Medicine/Basic Science Departments/Biochemistry
pubs.organisational-group /Duke/School of Medicine/Basic Science Departments/Cell Biology
pubs.organisational-group /Duke/School of Medicine/Basic Science Departments/Molecular Genetics and Microbiology
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments/Medicine
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments/Medicine/Medicine, Cardiology
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments/Pathology
pubs.organisational-group /Duke/School of Medicine/Institutes and Centers
pubs.organisational-group /Duke/School of Medicine/Institutes and Centers/Duke Cancer Institute
pubs.organisational-group /Duke/Trinity College of Arts & Sciences
pubs.organisational-group /Duke/Trinity College of Arts & Sciences/Chemistry
pubs.publication-status Published
pubs.volume 115

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