Linked Life Data

11334883

Source:http://linkedlifedata.com/resource/pubmed/id/11334883

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2001-5-3
pubmed:abstractText
We tested the hypothesis that specific isoforms of protein kinase C (PKC) are responsible for modulation of Na+ current (I(Na)) derived from the human cardiac Na+ channel using activators and inhibitors selective for specific PKCs. Experimental results demonstrated that I(Na) suppression was mediated by activation of conventional PKCs (cPKCs) and possibly resulted from channel internalization. In the presence of cPKC inhibition, phorbol ester application unexpectedly increased Na+ current, an effect eliminated by inhibition of protein kinase A. These findings demonstrate complex modulation of cardiac I(Na) by protein kinases and provide further evidence that PKC isoforms have distinct protein targets.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0014-5793
pubmed:author
pubmed:issnType
Print
pubmed:day
27
pubmed:volume
495
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
154-8
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Conventional protein kinase C isoforms and cross-activation of protein kinase A regulate cardiac Na+ current.
pubmed:affiliation
Department of Pharmacology, Vanderbilt University School of Medicine, Room 559 Preston Research Building, 23rd and Pierce Avenues, Nashville, TN 37232-6602, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.