Linked Life Data

17459908

Source:http://linkedlifedata.com/resource/pubmed/id/17459908

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-8-1
pubmed:abstractText
Here we review the considerable body of evidence that has accumulated to support the notion of S100A1, a cardiac-specific Ca(2+)-sensor protein of the EF-hand type, as a physiological regulator of excitation-contraction coupling and inotropic reserve mechanisms in the mammalian heart. In particular, molecular mechanisms will be discussed conveying the Ca(2+)-dependent inotropic actions of S100A1 protein in cardiomyocytes occurring independently of beta-adrenergic signaling. Moreover, we will shed light on the molecular structure-function relationship of S100A1 with its cardiac target proteins at the sarcoplasmic reticulum, the sarcomere, and the mitochondria. Furthermore, pathophysiological consequences of disturbed S100A1 protein expression on altered Ca(2+) handling and intertwined systems in failing myocardium will be highlighted. Subsequently, therapeutic options by means of genetic manipulation of cardiac S100A1 expression will be discussed, aiming to complete our current understanding of the role of S100A1 in diseased myocardium.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0363-6119
pubmed:author
pubmed:issnType
Print
pubmed:volume
293
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
R568-77
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
S100A1: a novel inotropic regulator of cardiac performance. Transition from molecular physiology to pathophysiological relevance.
pubmed:affiliation
Center for Translational Medicine, Laboratory for Cardiac Stem Cell and Gene Therapy, Department of Medicine, Thomas Jefferson University, Philadelphia, PA 19107, USA. patrick.most@jefferson.edu
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural