Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1994-4-26
pubmed:abstractText
Incubation of mammalian cells in medium containing low K+ is often associated with an increase in Na,K-ATPase activity and content. In the present studies, we investigated the effect of low K+ on the regulation of Na,K-ATPase alpha 1 and beta 1 gene expression in primary cultures of neonatal rat cardiac myocytes. Northern blot hybridization analysis indicated that exposure of cardiocytes to a medium containing 0.3 mmol/L K+ for 72 h resulted in 1.8- and 3.3-fold increases in the abundance of alpha 1 and beta 1 mRNAs, respectively, compared with control cells exposed to 5.4 mmol/L K+. To investigate the molecular mechanism of the low K effect on beta 1 mRNA content, we constructed chimeric genes with a full-length and deleted portion of the 5' end of the rat beta 1 gene linked to the firefly luciferase gene. Transient transfection experiments using these constructs indicated that beta 1 gene sequences between -102 and +151 base pairs (bp) are required for low K(+)-induced trans-activation of reporter gene expression. Taken together, these results indicate that low K+ induction of beta 1 mRNA abundance in neonatal rat cardiac myocytes is mediated by regulatory DNA sequences in close proximity to the site of transcription initiation of the beta 1 gene.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0895-7061
pubmed:author
pubmed:issnType
Print
pubmed:volume
7
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
96-9
pubmed:dateRevised
2009-2-24
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Low external K+ regulates Na,K-ATPase alpha 1 and beta 1 gene expression in rat cardiac myocytes.
pubmed:affiliation
Department of Biochemistry, State University of New York Health Science Center at Brooklyn 11203.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't