rdf:type |
|
lifeskim:mentions |
umls-concept:C0010531,
umls-concept:C0013081,
umls-concept:C0026844,
umls-concept:C0034787,
umls-concept:C0035696,
umls-concept:C0037083,
umls-concept:C0205147,
umls-concept:C0439851,
umls-concept:C1514248,
umls-concept:C1552596,
umls-concept:C1710082,
umls-concept:C1947931
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pubmed:issue |
11
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pubmed:dateCreated |
2000-4-12
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pubmed:abstractText |
Cell surface receptor activation generally leads to changes in mRNA abundance, which may involve regulatory targets in processes working at the post-transcriptional level. Many types of agonists down-regulate vascular smooth muscle angiotensin receptor (AT(1)-R) gene expression, but it is unclear which of these activate post-transcriptional mechanisms. To reconstitute faithfully the normal AT(1)-R mRNA regulatory environment, tetracycline-suppressible promoters drive highly accurate recombinant AT(1)-R mRNA mimics in vascular smooth muscle cells that co-express an endogenous AT(1)-R mRNA. Down-regulation of the latter occurs shortly after stimulating mitogenic receptors or by using forskolin, but only cAMP signaling reduces expression of the recombinant AT(1)-R mRNA. Transcription of the recombinant mRNA is unaffected by cAMP signaling. Deletions of the AT(1)-R mRNA 3'-untranslated region do not impair cAMP-mediated down-regulation. Both loss of function and gain of function mutants show the response is mediated by the 5'-untranslated region. These observations provide the first direct functional evidence for modulation of vascular AT(1)-R gene expression by a mechanism involving a protein kinase A-regulated post-transcriptional process.
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pubmed:grant |
|
pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/5a,6-anhydrotetracycline,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP-Dependent Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Forskolin,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogens,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Angiotensin, Type 1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Angiotensin, Type 2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Angiotensin,
http://linkedlifedata.com/resource/pubmed/chemical/Tetracyclines,
http://linkedlifedata.com/resource/pubmed/chemical/Untranslated Regions
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
|
pubmed:issn |
0021-9258
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:day |
17
|
pubmed:volume |
275
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
7604-11
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:10713068-Animals,
pubmed-meshheading:10713068-Aorta,
pubmed-meshheading:10713068-Cells, Cultured,
pubmed-meshheading:10713068-Cyclic AMP-Dependent Protein Kinases,
pubmed-meshheading:10713068-Down-Regulation,
pubmed-meshheading:10713068-Forskolin,
pubmed-meshheading:10713068-Half-Life,
pubmed-meshheading:10713068-Mitogens,
pubmed-meshheading:10713068-Mitosis,
pubmed-meshheading:10713068-Muscle, Smooth, Vascular,
pubmed-meshheading:10713068-Mutation,
pubmed-meshheading:10713068-RNA, Messenger,
pubmed-meshheading:10713068-RNA Processing, Post-Transcriptional,
pubmed-meshheading:10713068-RNA Stability,
pubmed-meshheading:10713068-Rats,
pubmed-meshheading:10713068-Receptor, Angiotensin, Type 1,
pubmed-meshheading:10713068-Receptor, Angiotensin, Type 2,
pubmed-meshheading:10713068-Receptors, Angiotensin,
pubmed-meshheading:10713068-Signal Transduction,
pubmed-meshheading:10713068-Tetracyclines,
pubmed-meshheading:10713068-Untranslated Regions
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pubmed:year |
2000
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pubmed:articleTitle |
Reconstitution of angiotensin receptor mRNA down-regulation in vascular smooth muscle. Post-transcriptional control by protein kinase a but not mitogenic signaling directed by the 5'-untranslated region.
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pubmed:affiliation |
Department of Pharmacology, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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