Linked Life Data

15304358

Source:http://linkedlifedata.com/resource/pubmed/id/15304358

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-3
pubmed:dateCreated
2004-8-12
pubmed:abstractText
Sodium channel Na(v)1.8 requires stronger depolarization than other sodium channels for activation and inactivation. The contribution of Na(v)1.8 C-terminus to this property was investigated by producing Na(v)1.8 and Na(v)1.4 chimeras and expressing them in ND7/23 cells. Current densities of the chimeras were significantly different than in parental channels, and the voltage-dependence of activation was depolarized in Na(v)1.4/1.8C compared to Na(v)1.4. Analysis of steady-state inactivation showed that only Na(v)1.8 and Na(v)1.4/1.8C currents demonstrate a non-inactivated fraction. Thus, the C-terminus of Na(v)1.8 contributes to regulation of channel density at the cell surface, modulates channel gating, and regulates the generation of sustained current.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0014-5793
pubmed:author
pubmed:issnType
Print
pubmed:day
13
pubmed:volume
572
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
256-60
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Functional role of the C-terminus of voltage-gated sodium channel Na(v)1.8.
pubmed:affiliation
Department of Neurology, Yale University School of Medicine, New Haven CT 06510, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't