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rdf:type |
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lifeskim:mentions |
umls-concept:C0009015,
umls-concept:C0013879,
umls-concept:C0025914,
umls-concept:C0026809,
umls-concept:C0035820,
umls-concept:C0040649,
umls-concept:C0086222,
umls-concept:C0086860,
umls-concept:C0225828,
umls-concept:C0285965,
umls-concept:C0936012,
umls-concept:C1145667,
umls-concept:C1335671,
umls-concept:C1420679,
umls-concept:C1705733,
umls-concept:C1825950,
umls-concept:C1880022
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pubmed:issue |
5
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pubmed:dateCreated |
2001-4-18
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pubmed:databankReference |
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pubmed:abstractText |
alpha1-Adrenergic receptor (AR) subtypes in the heart are expressed by myocytes but not by fibroblasts, a feature that distinguishes alpha1-ARs from beta-ARs. Here we studied myocyte-specific expression of alpha1-ARs, focusing on the subtype alpha1C (also called alpha1A), a subtype implicated in cardiac hypertrophic signaling in rat models. We first cloned the mouse alpha1C-AR gene, which consisted of two exons with an 18 kb intron, similar to the alpha1B-AR gene. The receptor coding sequence was >90% homologous to that of rat and human. alpha1C-AR transcription in mouse heart was initiated from a single Inr consensus sequence at -588 from the ATG; this and a putative polyadenylation sequence 8.5 kb 3' could account for the predominant 11 kb alpha1C mRNA in mouse heart. A 5'-nontranscribed fragment of 4.4 kb was active as a promoter in cardiac myocytes but not in fibroblasts. Promoter activity in myocytes required a single muscle CAT (MCAT) element, and this MCAT bound in vitro to recombinant and endogenous transcriptional enhancer factor-1. Thus, alpha1C-AR transcription in cardiac myocytes shares MCAT dependence with other cardiac-specific genes, including the alpha- and beta-myosin heavy chains, skeletal alpha-actin, and brain natriuretic peptide. However, the mouse alpha1C gene was not transcribed in the neonatal heart and was not activated by alpha1-AR and other hypertrophic agonists in rat myocytes, and thus differed from other MCAT-dependent genes and the rat alpha1C gene.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Chloramphenicol O-Acetyltransferase,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Norepinephrine,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, alpha-1,
http://linkedlifedata.com/resource/pubmed/chemical/Tead1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0026-895X
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
59
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1225-34
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:11306707-Amino Acid Sequence,
pubmed-meshheading:11306707-Animals,
pubmed-meshheading:11306707-Chloramphenicol O-Acetyltransferase,
pubmed-meshheading:11306707-Cloning, Molecular,
pubmed-meshheading:11306707-DNA-Binding Proteins,
pubmed-meshheading:11306707-Gene Expression Regulation,
pubmed-meshheading:11306707-Heart,
pubmed-meshheading:11306707-Mice,
pubmed-meshheading:11306707-Molecular Sequence Data,
pubmed-meshheading:11306707-Myocardium,
pubmed-meshheading:11306707-Norepinephrine,
pubmed-meshheading:11306707-Promoter Regions, Genetic,
pubmed-meshheading:11306707-RNA, Messenger,
pubmed-meshheading:11306707-Receptors, Adrenergic, alpha-1,
pubmed-meshheading:11306707-Response Elements,
pubmed-meshheading:11306707-Sequence Homology, Amino Acid,
pubmed-meshheading:11306707-Transcription, Genetic,
pubmed-meshheading:11306707-Transcription Factors
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pubmed:year |
2001
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pubmed:articleTitle |
Cloning and characterization of the mouse alpha1C/A-adrenergic receptor gene and analysis of an alpha1C promoter in cardiac myocytes: role of an MCAT element that binds transcriptional enhancer factor-1 (TEF-1).
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pubmed:affiliation |
Cardiology Division and Research Service, Veterans Affairs Medical Center, San Francisco, California, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
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