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| Subject | Predicate | Object |
|---|---|---|
| http://purl.uniprot.org/citations/18006496 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/18006496 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/18006496 | http://www.w3.org/2000/01/rdf-schema#comment | "Heptahelical G protein-coupled receptors employ several mechanisms to activate the ERK1/2 cascade and control gene transcription. Previous work with the angiotensin AT1a receptor has shown that G(q/11) activation leads to a rapid and transient rise in ERK1/2 activity, whereas beta-arrestin binding supports sustained ERK1/2 activation by scaffolding a Raf.MEK.ERK complex associated with the internalized receptor. In this study, we compared the role of the two beta-arrestin isoforms in AT1a receptor desensitization, ERK1/2 activation and transcription using selective RNA interference. In HEK293 cells, both the native AT1a receptor and a G protein-coupling deficient DRY/AAY mutant recruited beta-arrestin1 and beta-arrestin2 upon angiotensin binding and internalized with the receptor. In contrast, only beta-arrestin2 supported protein kinase C-independent ERK1/2 activation by both the AT1a and DRY/AAY receptors. Using focused gene expression filter arrays to screen for endogenous transcriptional responses, we found that silencing beta-arrestin1 or beta-arrestin2 individually did not alter the response pattern but that silencing both caused a marked increase in the number of transcripts that were significantly up-regulated in response to AT1a receptor activation. The DRY/AAY receptor failed to elicit any detectable transcriptional response despite its ability to stimulate beta-arrestin2-dependent ERK1/2 activation. These results indicate that the transcriptional response to AT1a receptor activation primarily reflects heterotrimeric G protein activation. Although beta-arrestin1 and beta-arrestin2 are functionally specialized with respect to supporting G protein-independent ERK1/2 activation, their common effect is to dampen the transcriptional response by promoting receptor desensitization."xsd:string |
| http://purl.uniprot.org/citations/18006496 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.m706892200"xsd:string |
| http://purl.uniprot.org/citations/18006496 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.m706892200"xsd:string |
| http://purl.uniprot.org/citations/18006496 | http://purl.uniprot.org/core/author | "Lee M.-H."xsd:string |
| http://purl.uniprot.org/citations/18006496 | http://purl.uniprot.org/core/author | "Lee M.-H."xsd:string |
| http://purl.uniprot.org/citations/18006496 | http://purl.uniprot.org/core/author | "Luttrell D.K."xsd:string |
| http://purl.uniprot.org/citations/18006496 | http://purl.uniprot.org/core/author | "Luttrell D.K."xsd:string |
| http://purl.uniprot.org/citations/18006496 | http://purl.uniprot.org/core/author | "Luttrell L.M."xsd:string |
| http://purl.uniprot.org/citations/18006496 | http://purl.uniprot.org/core/author | "Luttrell L.M."xsd:string |
| http://purl.uniprot.org/citations/18006496 | http://purl.uniprot.org/core/author | "El-Shewy H.M."xsd:string |
| http://purl.uniprot.org/citations/18006496 | http://purl.uniprot.org/core/author | "El-Shewy H.M."xsd:string |
| http://purl.uniprot.org/citations/18006496 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
| http://purl.uniprot.org/citations/18006496 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
| http://purl.uniprot.org/citations/18006496 | http://purl.uniprot.org/core/name | "J. Biol. Chem."xsd:string |
| http://purl.uniprot.org/citations/18006496 | http://purl.uniprot.org/core/name | "J. Biol. Chem."xsd:string |
| http://purl.uniprot.org/citations/18006496 | http://purl.uniprot.org/core/pages | "2088-2097"xsd:string |
| http://purl.uniprot.org/citations/18006496 | http://purl.uniprot.org/core/pages | "2088-2097"xsd:string |
| http://purl.uniprot.org/citations/18006496 | http://purl.uniprot.org/core/title | "Role of beta-arrestin-mediated desensitization and signaling in the control of angiotensin AT1a receptor-stimulated transcription."xsd:string |
| http://purl.uniprot.org/citations/18006496 | http://purl.uniprot.org/core/title | "Role of beta-arrestin-mediated desensitization and signaling in the control of angiotensin AT1a receptor-stimulated transcription."xsd:string |
| http://purl.uniprot.org/citations/18006496 | http://purl.uniprot.org/core/volume | "283"xsd:string |
| http://purl.uniprot.org/citations/18006496 | http://purl.uniprot.org/core/volume | "283"xsd:string |
| http://purl.uniprot.org/citations/18006496 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/18006496 |
| http://purl.uniprot.org/citations/18006496 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/18006496 |