Linked Life Data

17967416

Source:http://linkedlifedata.com/resource/pubmed/id/17967416

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2007-11-20
pubmed:abstractText
Kir3.4 and Kir3.1 potassium channel subunits mediate the acetylcholine induced inwardly rectifying current I(KACh) in the heart. We found a glycine to arginine substitution in codon 247 of Kir3.4 in a patient with a single episode of atrial fibrillation (AF). Expression in Xenopus laevis oocytes and two-electrode voltage-clamp revealed that Kir3.4-G247R basal current was reduced compared to wild-type Kir3.4 and co-expression with the muscarinic acetylcholine receptor type 2 showed that also the acetylcholine induced current was severely reduced in Kir3.4-G247R, indicating that the mutation interfered with activation by the stimulatory G betagamma-subunits. Co-expression of Kir3.4-G247R with wild-type Kir3.4 or Kir3.1 had a compensating effect on both basal current levels and the response to muscarinic stimulation suggesting the function of Kir3.4-G247R is compensated in vivo. This may explain the lack of clear clinical manifestations and further studies are necessary to elucidate if mutations in Kir3.4 are predisposing AF.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1090-2104
pubmed:author
pubmed:issnType
Electronic
pubmed:day
28
pubmed:volume
364
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
889-95
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Characterizations of a loss-of-function mutation in the Kir3.4 channel subunit.
pubmed:affiliation
The Danish National Research Foundation Centre for Cardiac Arrhythmia, Department of Biomedical Sciences, 12.5.10, University of Copenhagen, Blegdamsvej 3, 2200 Copenhagen N, Denmark. Kirstinec@mfi.ku.dk
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't