Linked Life Data

8798397

Source:http://linkedlifedata.com/resource/pubmed/id/8798397

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
37
pubmed:dateCreated
1996-11-7
pubmed:abstractText
Calcium stores from cultured skeletal muscle cells were depleted using cyclopiazonic acid (CPA), a reversible inhibitor of Ca2+-ATPases at the sarcoplasmic reticulum. Store depletion led to activation of the calcium-specific leak channel, as assayed using single-channel patch clamp analysis and rates of manganese influx and quenching of fura-2 fluorescence. Two novel dihydropyridine compounds inhibited this single-channel leak channel activity, the resting and depletion-induced manganese influx, and refilling of the CPA-depleted intracellular calcium store. These compounds represent the first antagonists for a calcium leak channel and for a channel that mediates a capacitative current. The development of the skeletal muscle capacitative current was inhibited by genistein, a tyrosine kinase inhibitor, but was not affected by okadaic acid, a phosphatase inhibitor, or econazole. Thus, the capacitative current in cultured skeletal muscle cells was mediated by the calcium leak channel and was inhibited by pharmacological antagonists and may provide a model system for uncovering the complete set of signals leading from store depletion to channel activation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
13
pubmed:volume
271
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
22358-67
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
A capacitative calcium current in cultured skeletal muscle cells is mediated by the calcium-specific leak channel and inhibited by dihydropyridine compounds.
pubmed:affiliation
Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley, California, 94720, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't