AbstractMyocyte-specific enhancer factor 2A (MEF2A) regulates a broad range of fundamental cellular processes including cell division, differentiation and death. Here, we tested the hypothesis that MEF2A is required in cardiac contractility employing zebrafish as a model organism. MEF2A is highly expressed in heart as well as somites during zebrafish embryogenesis. Knock-down of MEF2A in zebrafish impaires the cardiac contractility and results in sarcomere assembly defects. Dysregulation of cardiac genes in MEF2A morphants suggests that sarcomere assembly disturbances account for the cardiac contractile deficiency. Our studies suggested that MEF2A is essential in cardiac contractility
AbstractAn outstanding problem in vertebrate development has been to define the genetic program that...
Background-Sudden cardiac death due to malignant ventricular arrhythmia is a devastating manifestati...
Cardiovascular malformations (CVMs) have a higher incidence in patients with NF1 microdeletion syndr...
AbstractMyocyte-specific enhancer factor 2A (MEF2A) regulates a broad range of fundamental cellular ...
SummaryMef2 transcription factors have been strongly linked with early heart development. D-mef2 is ...
SummaryMef2 transcription factors have been strongly linked with early heart development. D-mef2 is ...
AbstractVarious hypotheses have been proposed to explain the molecule processes of sarcomere assembl...
Congenital heart diseases (CHDs) are the most common type of human birth defect and often feature st...
The heart responds to stress signals by hypertrophic growth, which is the first step towards heart f...
The heart responds to stress signals by hypertrophic growth, which is the first step towards heart f...
AbstractThe specification of an appropriate number of cardiomyocytes from the lateral plate mesoderm...
In humans, myocardial infarction results in ventricular remodeling, progressing ultimately to cardia...
The family of vertebrate Mef2 transcription factors is comprised of four members named Mef2a, Mef2b,...
In humans, myocardial infarction results in ventricular remodeling, progressing ultimately to cardia...
Proper formation of the mammalian heart requires precise spatiotemporal transcriptional regulation o...
AbstractAn outstanding problem in vertebrate development has been to define the genetic program that...
Background-Sudden cardiac death due to malignant ventricular arrhythmia is a devastating manifestati...
Cardiovascular malformations (CVMs) have a higher incidence in patients with NF1 microdeletion syndr...
AbstractMyocyte-specific enhancer factor 2A (MEF2A) regulates a broad range of fundamental cellular ...
SummaryMef2 transcription factors have been strongly linked with early heart development. D-mef2 is ...
SummaryMef2 transcription factors have been strongly linked with early heart development. D-mef2 is ...
AbstractVarious hypotheses have been proposed to explain the molecule processes of sarcomere assembl...
Congenital heart diseases (CHDs) are the most common type of human birth defect and often feature st...
The heart responds to stress signals by hypertrophic growth, which is the first step towards heart f...
The heart responds to stress signals by hypertrophic growth, which is the first step towards heart f...
AbstractThe specification of an appropriate number of cardiomyocytes from the lateral plate mesoderm...
In humans, myocardial infarction results in ventricular remodeling, progressing ultimately to cardia...
The family of vertebrate Mef2 transcription factors is comprised of four members named Mef2a, Mef2b,...
In humans, myocardial infarction results in ventricular remodeling, progressing ultimately to cardia...
Proper formation of the mammalian heart requires precise spatiotemporal transcriptional regulation o...
AbstractAn outstanding problem in vertebrate development has been to define the genetic program that...
Background-Sudden cardiac death due to malignant ventricular arrhythmia is a devastating manifestati...
Cardiovascular malformations (CVMs) have a higher incidence in patients with NF1 microdeletion syndr...