Linked Life Data

20708651

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

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pubmed-article:20708651pubmed:dateCreated2010-11-15lld:pubmed
pubmed-article:20708651pubmed:abstractTextThe 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.lld:pubmed
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pubmed-article:20708651pubmed:authorpubmed-author:KnudsenSteenSlld:pubmed
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pubmed-article:20708651pubmed:authorpubmed-author:SchneiderMika...lld:pubmed
pubmed-article:20708651pubmed:copyrightInfoCopyright © 2010 Elsevier Ireland Ltd. All rights reserved.lld:pubmed
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pubmed-article:20708651pubmed:pagination49-56lld:pubmed
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pubmed-article:20708651pubmed:year2011lld:pubmed
pubmed-article:20708651pubmed:articleTitleAT(1) receptor G?q protein-independent signalling transcriptionally activates only a few genes directly, but robustly potentiates gene regulation from the ?2-adrenergic receptor.lld:pubmed
pubmed-article:20708651pubmed:affiliationLaboratory for Molecular Cardiology, Danish National Research Foundation Centre for Cardiac Arrhythmia, Department of Biomedical Sciences, University of Copenhagen, Blegdamsvej 3b, DK-2200 Copenhagen, Denmark.lld:pubmed
pubmed-article:20708651pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:20708651pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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