Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1996-9-23
pubmed:abstractText
Most of the patients with congenital heart diseases express the atrial myosin light chain 1 (ALC-1) in the right ventricle. We investigated the functional consequences of ALC-1 expression on the myosin cycling kinetics in the intact sarcomeric structure using multicellular demembranated fibers ("skinned fibers") from the right ventricular infundibulum of patients with Tetralogy of Fallot (TOF), double outlet right ventricle (DORV), and infundibular pulmonary stenosis (IPS), Force-velocity relation was analyzed by the constant-load technique at maximal Ca2+ activation (pCa 4.5). Half-time of tension development (t1/2) was investigated by monitoring contraction initiation upon photolytic release of ATP from caged-ATP in rigor. The patients investigated here expressed between 0 and 27% ALC-1. There was a statistically significant correlation between ALC-l and maximal shortening velocity (Vmax) which rose 1.87-fold from 1.2 muscle length per second (ML/s) to 2.25 ML/s in a normal (0% ALC-1) and diseased (19.9% ALC-1) ventricle. Half-time of tension development decreased 1.85-fold with increasing ALC-1 expression (t1/2) was 0.252 s and 0.136 s at 2 and 18.4% ALC-1, respectively). We conclude that the expression of ALC-1 in the human heart modulates cross-bridge cycling kinetics accelerating shortening velocity and isometric tension production.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-125404, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-13485191, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-1403812, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-1533180, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-2308163, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-2764861, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-2942954, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-2966401, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-3037493, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-3156404, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-3190654, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-3303962, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-3342480, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-3379059, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-3417683, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-3549306, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-3621284, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-3719931, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-3840099, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-3871943, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-3904738, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-4838672, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-4942892, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-4942893, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-533865, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-6092382, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-6241906, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-6304733, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-6585819, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-6938971, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-7115691, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-7236212, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-7572232, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-7623850, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-7728988, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-7858130, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-7965849, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-8316857, http://linkedlifedata.com/resource/pubmed/commentcorrection/8755658-8508533
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0021-9738
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
98
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
467-73
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed-meshheading:8755658-Adenosine Triphosphate, pubmed-meshheading:8755658-Blood Pressure, pubmed-meshheading:8755658-Calcium, pubmed-meshheading:8755658-Child, pubmed-meshheading:8755658-Child, Preschool, pubmed-meshheading:8755658-Female, pubmed-meshheading:8755658-Heart, pubmed-meshheading:8755658-Heart Defects, Congenital, pubmed-meshheading:8755658-Heart Ventricles, pubmed-meshheading:8755658-Homeostasis, pubmed-meshheading:8755658-Humans, pubmed-meshheading:8755658-Infant, pubmed-meshheading:8755658-Kinetics, pubmed-meshheading:8755658-Male, pubmed-meshheading:8755658-Middle Aged, pubmed-meshheading:8755658-Muscle, Smooth, Vascular, pubmed-meshheading:8755658-Myocardial Contraction, pubmed-meshheading:8755658-Myosin Light Chains, pubmed-meshheading:8755658-Pulmonary Artery, pubmed-meshheading:8755658-Pulmonary Valve Stenosis, pubmed-meshheading:8755658-Reference Values, pubmed-meshheading:8755658-Tetralogy of Fallot
pubmed:year
1996
pubmed:articleTitle
Regulation of human heart contractility by essential myosin light chain isoforms.
pubmed:affiliation
Max-Delbrück-Center for Molecular Medicine, Berlin, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't