Linked Life Data

20708651

Source:http://linkedlifedata.com/resource/pubmed/id/20708651

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2010-11-15
pubmed:abstractText
The angiotensin II type 1 receptor (AT(1)R) is known to signal through heterotrimeric G proteins, and G?q protein-independent signalling has only recently gained appreciation for profound impact on a diverse range of biological functions. ?-Arrestins, among other central mediators of G?q protein-independent signalling from the AT(1)R interact with transcriptional regulators and promote phosphorylation of nuclear proteins. However, the relative contribution of G?q protein-independent signalling in AT(1)R mediated transcriptional regulation remains elusive. We here present a comprehensive comparative analysis of G?q protein-dependent and -independent regulation of AT(1)R mediated gene expression. We found angiotensin II to regulate 212 genes, whereas G?q-independent signalling obtained with the biased agonist, SII angiotensin II only regulated few genes. Interestingly, SII angiotensin II, like Ang II vastly potentiated ?2-adrenergic receptor-stimulated gene expression. These novel findings indicate that the G?q protein-independent signalling mainly modifies the transcriptional response governed by other signalling pathways, while direct induction of gene expression by the AT(1)R is dependent on classical G?q protein activation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1872-8057
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
331
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
49-56
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
AT(1) receptor G?q protein-independent signalling transcriptionally activates only a few genes directly, but robustly potentiates gene regulation from the ?2-adrenergic receptor.
pubmed:affiliation
Laboratory for Molecular Cardiology, Danish National Research Foundation Centre for Cardiac Arrhythmia, Department of Biomedical Sciences, University of Copenhagen, Blegdamsvej 3b, DK-2200 Copenhagen, Denmark.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't