Linked Life Data

10494839

Source:http://linkedlifedata.com/resource/pubmed/id/10494839

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7-8
pubmed:dateCreated
1999-10-19
pubmed:abstractText
Ca2+ influx through high voltage activated Ca2+ channels initiates a number of physiological processes including e.g. excitation-contraction coupling in cardiac myocytes and excitation-transcription coupling in neurones. The Ca2+ channels involved are complexes of a pore-forming alpha1 subunit, a transmembrane delta subunit disulfide-linked to an extracellular alpha2 subunit, a intracellular beta subunit and, at least in some tissues, a gamma subunit. Experimental analysis of beta subunit function comprises functional coexpression of its cDNA together with the cDNAs of the other subunits. This experimental approach can be supplemented by investigating functional alterations that result from the genetic elimination of Ca2+ channel beta genes in mice. Here we summarize the phenotype of mice deficient in the beta1 subunit, the beta3 subunit or the beta4 subunit, respectively.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1431-6730
pubmed:author
pubmed:issnType
Print
pubmed:volume
380
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
897-902
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:articleTitle
Mutations of calcium channel beta subunit genes in mice.
pubmed:affiliation
Institut für Pharmakologie und Toxikologie, Universität des Saarlandes, Homburg, Germany.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't