Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1993-2-11
pubmed:abstractText
To explore the mechanisms regulating expression of ventricular myosin light chain 1, the human gene including 5'-flanking DNA was cloned and characterized by Southern blot and restriction mapping. A 2 kb 5'-flanking DNA was sequenced and linked to a chloramphenicol acetyltransferase reporter gene. The constructs then were transfected into cultured human and rat cardiomyocytes as well as rat aortic endothelial cells. Deletion analysis of constructs revealed that the basal promoter sequences, which were located within 62 base pairs of the cap site, could direct high levels of chloramphenicol acetyltransferase gene expression in the cardiomyocytes and endothelial cells. The region between -62 to -312 base pairs strongly repressed the chloramphenicol acetyltransferase gene expression in the cardiomyocytes and endothelial cells. Positive elements were found between -312 and -2000 base pairs of the cap site. These results are indicative, among other possibilities, that the human ventricular myosin light chain 1 gene is turned on in cardiomyocytes by the presence of trans-acting factors that are bound to upstream positive elements and is turned off in non-muscle cells by the presence of repressor-binding proteins. But this mechanism remains to be established.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-2828
pubmed:author
pubmed:issnType
Print
pubmed:volume
24
pubmed:geneSymbol
VMLC1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1221-9
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Analysis of the upstream regulatory region of human ventricular myosin light chain 1 gene.
pubmed:affiliation
Toronto Hospital-General Division, Ontario, Canada.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't