Linked Life Data

19763850

Source:http://linkedlifedata.com/resource/pubmed/id/19763850

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5-6
pubmed:dateCreated
2010-1-21
pubmed:abstractText
Secophalloidin (SPH) is known to cause in cardiac myofibrils force without Ca(2+) (half-maximal effect approximately 2 mM) followed by irreversible loss of Ca(2+)-activated force. At maximal Ca(2+) activation, SPH increases force (half-maximal effect < 0.1 mM). We found that SPH at low concentration (0.5 mM) did not cause either force activation or force loss at pCa 8.7, but both of these effects did occur when force was activated by Ca(2+). The force loss was prevented when SPH was applied during rigor or in the presence of 2,3-butanedione monoxime (85 mM). Furthermore, studying muscle in which the force was previously reduced by SPH (up to 50%) did not reveal significant changes in Ca(2+) sensitivity and cooperativity of Ca(2+) activation or qualitative alterations in SPH-induced changes in Ca(2+)-activated contraction. Data suggest that the force loss is mediated by cycling cross-bridges, and might reflect a reduction in force generated by individual cross-bridges.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1573-2657
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
30
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
209-16
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Characterization of secophalloidin-induced force loss in cardiac myofibrils.
pubmed:affiliation
Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, Scottsdale, AZ 85259, USA. boukatina.anna@mayo.edu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural