Linked Life Data

10205154

Source:http://linkedlifedata.com/resource/pubmed/id/10205154

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1999-4-30
pubmed:abstractText
The aims of the present studies were to define sufficient promoter sequences required to drive endogenous expression of smooth muscle (SM) alpha-actin and to determine whether regulation of SM alpha-actin expression in vivo is dependent on CArG (CC(A/T)6GG) cis elements. Promoter deletions and site directed mutagenesis techniques were used to study gene regulation in transgenic mice as well as in smooth muscle cell (SMC) cultures. Results demonstrated that a Lac Z transgene that contained 547 bp of the 5' rat SM alpha-actin promoter was sufficient to drive embryonic expression of SM alpha-actin in the heart and in skeletal muscle but not in SMCs. Transient transfections into SMC cultures demonstrated that the conserved CArG element in the first intron had significant positive activity, and gel shift analyses demonstrated that the intronic CArG bound serum response factor. A transgene construct from -2600 through the first intron (p2600Int/Lac Z) was expressed in embryos and adults in a pattern that closely mimicked endogenous SM alpha-actin expression. Expression in adult mice was completely restricted to SMCs and was detected in esophagus, stomach, intestine, lung, and nearly all blood vessels, including coronary, mesenteric, and renal vascular beds. Mutation of CArG B completely inhibited expression in all cell types, whereas mutation of the intronic CArG selectively abolished expression in SMCs, which suggests that it may act as an SMC-specific enhancer-like element. Taken together, these results provide the first in vivo evidence for the importance of multiple CArG cis elements in the regulation of SM alpha-actin expression.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0009-7330
pubmed:author
pubmed:issnType
Print
pubmed:day
16
pubmed:volume
84
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
852-61
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:10205154-Actins, pubmed-meshheading:10205154-Animals, pubmed-meshheading:10205154-Aorta, Thoracic, pubmed-meshheading:10205154-Cells, Cultured, pubmed-meshheading:10205154-DNA-Binding Proteins, pubmed-meshheading:10205154-Gene Expression Regulation, Developmental, pubmed-meshheading:10205154-Genes, Reporter, pubmed-meshheading:10205154-Heart, pubmed-meshheading:10205154-Heterogeneous-Nuclear Ribonucleoprotein Group A-B, pubmed-meshheading:10205154-Introns, pubmed-meshheading:10205154-Lac Operon, pubmed-meshheading:10205154-Mice, pubmed-meshheading:10205154-Mice, Inbred C57BL, pubmed-meshheading:10205154-Mice, Transgenic, pubmed-meshheading:10205154-Muscle, Skeletal, pubmed-meshheading:10205154-Muscle, Smooth, Vascular, pubmed-meshheading:10205154-Mutagenesis, pubmed-meshheading:10205154-Plasmids, pubmed-meshheading:10205154-Promoter Regions, Genetic, pubmed-meshheading:10205154-Rats, pubmed-meshheading:10205154-Repressor Proteins, pubmed-meshheading:10205154-Transcriptional Activation, pubmed-meshheading:10205154-Transfection, pubmed-meshheading:10205154-Transgenes
pubmed:year
1999
pubmed:articleTitle
Regulation of smooth muscle alpha-actin expression in vivo is dependent on CArG elements within the 5' and first intron promoter regions.
pubmed:affiliation
Department of Molecular Physiology and Biological Physics, University of Virginia Medical School, Charlottesville, VA, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't