Linked Life Data

17051347

Source:http://linkedlifedata.com/resource/pubmed/id/17051347

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2006-10-31
pubmed:abstractText
In order to incorporate human cardiac troponin I (TnI) and troponin C (TnC) into guinea pig skinned cardiac trabeculae, fibres were treated with vanadate to extract endogenous TnI and TnC using established protocols. After addition of human TnI and TnC force was inadequately restored and it was found that the vanadate treatment had unexpectedly also removed some troponin T. To recover Ca(2+)-sensitive force, the fibres had to be incubated with all three troponin subunits. Using this revised method, the hypertrophic cardiomyopathy-causing mutation TnI Gly203Ser had no significant effect on Ca(2+)-sensitivity of force production, contrasting with our earlier report of decreased Ca(2+)-sensitivity which was likely caused by the unexpectedly harsh effect of vanadate.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0142-4319
pubmed:author
pubmed:issnType
Print
pubmed:volume
27
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
585-90
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
A revised method of troponin exchange in permeabilised cardiac trabeculae using vanadate: functional consequences of a HCM-causing mutation in troponin I.
pubmed:affiliation
Department of Cardiovascular Medicine, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford OX3 7BN, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't