Linked Life Data

10811658

Source:http://linkedlifedata.com/resource/pubmed/id/10811658

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
31
pubmed:dateCreated
2000-9-7
pubmed:abstractText
Expression of Na,K-ATPase activity is up-regulated in cells incubated for extended intervals in the presence of low external K(+). Our previous data showed that exposure of cardiac myocytes to low K(+) increased the steady-state abundance of Na,K-ATPase beta1 subunit mRNA. In the present study we determined that incubation of primary cultures of neonatal rat cardiac myocytes with low K(+) augmented Na,K-ATPase beta1 gene expression at a transcriptional level and that this effect required extracellular Ca(2+). The stimulatory effect of low K(+) on Na,K-ATPase beta1 gene transcription was not dependent on increased contractile activity of cardiac myocytes. Na,K-ATPase beta1 5'-flanking region deletion plasmids used in transient transfection analysis demonstrated that the region between nucleotides -62 to -42 of the beta1 promoter contained a low K(+) response element. Site-directed mutagenesis of a potential GC box core motif GCG in the -58/-56 region of the beta1 promoter decreased basal and low K(+)-mediated transcription. Mutation of the core sequence of a putative GC box element located between nucleotides -101 and -99 further decreased the low K(+) effect on beta1 gene transcription. Electrophoretic mobility shift assays using oligonucleotides spanning the proximal and distal GC box elements of the beta1 promoter showed enhanced binding of two complexes in response to low K(+). The inclusion of a consensus GC box sequence as a competitor in gel shift analysis reduced factor binding to the low K(+) response elements. Antibodies to transcription factors Sp1 and Sp3 interacted with components of both DNA-binding complexes and binding of nuclear factors was abolished in gel shift studies using GC box mutants. Together these data indicate that enhanced binding of Sp1 and Sp3 to two GC box elements in the rat Na,K-ATPase beta1 subunit gene promoter mediates beta1 gene transcription up-regulation in neonatal rat cardiac myocytes exposed to low external K(+).
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
4
pubmed:volume
275
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
24173-84
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:10811658-Animals, pubmed-meshheading:10811658-Base Sequence, pubmed-meshheading:10811658-Calcium, pubmed-meshheading:10811658-DNA-Binding Proteins, pubmed-meshheading:10811658-Gene Expression Regulation, Enzymologic, pubmed-meshheading:10811658-Heart, pubmed-meshheading:10811658-Male, pubmed-meshheading:10811658-Molecular Sequence Data, pubmed-meshheading:10811658-Mutation, pubmed-meshheading:10811658-Myocardial Contraction, pubmed-meshheading:10811658-Myocardium, pubmed-meshheading:10811658-Potassium, pubmed-meshheading:10811658-Promoter Regions, Genetic, pubmed-meshheading:10811658-Protein Binding, pubmed-meshheading:10811658-Rats, pubmed-meshheading:10811658-Rats, Sprague-Dawley, pubmed-meshheading:10811658-Regulatory Sequences, Nucleic Acid, pubmed-meshheading:10811658-Response Elements, pubmed-meshheading:10811658-Sequence Deletion, pubmed-meshheading:10811658-Sodium-Potassium-Exchanging ATPase, pubmed-meshheading:10811658-Sp1 Transcription Factor, pubmed-meshheading:10811658-Sp3 Transcription Factor, pubmed-meshheading:10811658-Transcription, Genetic, pubmed-meshheading:10811658-Transcription Factors
pubmed:year
2000
pubmed:articleTitle
Regulation of Na,K-ATPase beta 1 subunit gene transcription by low external potassium in cardiac myocytes. Role of Sp1 AND Sp3.
pubmed:affiliation
Department of Biochemistry and Center for Cardiovascular and Muscle Research, State University of New York Health Science Center at Brooklyn, Brooklyn, New York 11203, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't