Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
15
pubmed:dateCreated
2008-6-16
pubmed:abstractText
Inward rectifier potassium Kir2.x channels mediate cardiac inward rectifier potassium currents (I(K1)). As a subunit of Kir2.x, the physiological role of Kir2.3 in native cardiomyocytes has not been reported. This study shows that Kir2.3 knock-down remarkably down-regulates Kir2.3 expression (Kir2.3 protein was reduced to 19.91+/-3.24% on the 2nd or 3rd day) and I(K1) current densities (at -120 mV, control vs. knock-down: -5.03+/-0.24 pA/pF, n=5 vs. -1.16+/-0.19 pA/pF, n=7, P<0.001) in neonatal rat cardiomyocytes. The data suggest that Kir2.3 plays a potentially important role in I(K1) currents in neonatal rat cardiomyocytes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0014-5793
pubmed:author
pubmed:issnType
Print
pubmed:day
25
pubmed:volume
582
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2338-42
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Kir2.3 knock-down decreases IK1 current in neonatal rat cardiomyocytes.
pubmed:affiliation
Department of Cardiology, Tongji Hospital, Tongji University, Shanghai, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't