Depletion of zebrafish essential and regulatory myosin light chains reduces cardiac function through distinct mechanisms

Cardiovascular Research

Volumn 79, Issue 1, 2008, Pages 97-108

  Chen, Zhenyue ^a,b   Huang, Wei ^b   Dahme, Tillman ^c   Rottbauer, Wolfgang ^c   Ackerman, Michael J ^b,d   Xu, Xiaolei ^b  

^a SHANGHAI JIAO TONG UNIVERSITY SCHOOL OF MEDICINE   (China)

^b MAYO GRADUATE SCHOOL   (United States)

^c UNIVERSITY OF HEIDELBERG   (Germany)

^d Mayo Clinic   (United States)

Author keywords

Cardiomyopathy; Contractile apparatus; Contractile function; Hypertrophy; Ventricular function

Indexed keywords

MYOSIN LIGHT CHAIN;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CARDIOMYOPATHY; CELL COUNT; CELL SIZE; CONTROLLED STUDY; DISEASE COURSE; EMBRYO; GENE MUTATION; HEART FUNCTION; HEART MUSCLE CONTRACTILITY; HEART VENTRICLE FUNCTION; HEART VENTRICLE HYPERTROPHY; MUSCLE CELL; NONHUMAN; PRIORITY JOURNAL; PROTEIN DEPLETION; SARCOMERE LENGTH; ZEBRA FISH;

ANIMALS; CARDIAC MYOSINS; CARDIOMYOPATHIES; CELL COUNT; CELL SIZE; DISEASE MODELS, ANIMAL; HEART; MUTATION; MYOCARDIUM; MYOCYTES, CARDIAC; MYOSIN LIGHT CHAINS; OLIGORIBONUCLEOTIDES, ANTISENSE; SARCOMERES; ZEBRAFISH; ZEBRAFISH PROTEINS;

EID: 45849107907     PISSN: 00086363     EISSN: 17553245     Source Type: Journal    
DOI: 10.1093/cvr/cvn073     Document Type: Article

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