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variable transposon epigenetic silencing underlies the variable mef2ca mutant bone phenotype, and could be a widespread mechanism of phenotypic variability in animals.
Mef2 (zeige MYEF2 Proteine) controls skeletal muscle formation after terminal differentiation.
Our study provides new insights in MEF2C conservation and provides the first evidence of mef2cb regulation by both transcriptional and post transcriptional mechanisms.
By selectively inhibiting translational initiation of mef2ca and other mRNAs, eIF4EBP3L reprograms the translational profile of muscle, enabling it to adjust to new environmental conditions.
find no evidence that the phenotypic stability in the wild type is provided by redundancy between mef2ca and its co-ortholog mef2cb, or that it is related to the selector (homeotic) gene function of mef2ca
Mef2ca single mutants have delayed heart development, but form an apparently normal heart. Mef2cb single mutants have a functional heart and are viable adults.
Data show that mef2cb is expressed in the late ventricular region, and is necessary for late myocardial addition to the arterial pole.
the genetic interaction of Tbx5 (zeige TBX5 Proteine) and Mef2c is not only required for MYH6 (zeige MYH6 Proteine) expression but also essential for the early stages of heart development and survival
Mef2c and Mef2d (zeige MEF2D Proteine) are required for proper cardiac gene expression.
This study indicates MEF2C as a new gene responsible for human dilated cardiomyopathy (DCM), which provides novel insight into the mechanism underpinning DCM, suggesting potential implications for development of innovative prophylactic and therapeutic strategies for DCM, the most prevalent form of primary myocardial disease.
Overexpression of MEF2C decreased miR (zeige MLXIP Proteine)-448-induced VSMCs proliferation and migration.
MEF2C mRNA expression levels in AD subjects are significantly lower than those in control subjects and are correlated with disease severity.
The regulation mechanism of MIG6 (zeige ERRFI1 Proteine) and suggests potential implications for the therapeutic strategies of gefitinib resistance through inhibiting MEF2C in hepatic cancer cells.
This study firstly associates MEF2C loss-of-function mutation with double outlet right ventricle in humans, which provides novel insight into the molecular pathogenesis of congenital heart diseases.
Combined with automated 2D nano-scale chromatography, Accumulated ion monitoring achieved subattomolar limits of detection of endogenous proteins in complex biological proteomes. This allowed quantitation of absolute abundance of the human transcription factor MEF2C at approximately 100 molecules/cell, and determination of its phosphorylation stoichiometry from as little as 1 mug of extracts isolated from 10,000 human ...
the mutation significantly diminished the synergistic activation between MEF2C and GATA4 (zeige GATA4 Proteine), another cardiac core transcription factor that has been causally linked to Congenital heart disease (CHD (zeige CHDH Proteine)).
MEF2C expression levels were significantly associated with or may even be predictive of the response to glucocorticoid treatment.
MEF2C rs190982 polymorphism has a role in late-onset Alzheimer's disease in Han Chinese
MEF2C mRNA level is up-regulated in both sporadic and SOD1 + ALS patients.
Deletion and mutation analyses of the promoter of pig myocyte enhancer factor 2 (MEF2 (zeige MYEF2 Proteine)) gene showed that MyoD (zeige MYOD1 Proteine) and MEF2 (zeige MYEF2 Proteine) binding sites within the Mef2c promoter were responsible for the regulation of Mef2c transcription. This study helped to clarify the regulation of Mef2c in muscle differentiation and regeneration.
The cDNA sequence was analyzed and the 5' upstream region of the mef2c gene was isolated from porcine genomic DNA.
analysis of sequence and variations of the bovine myocyte enhancer factor 2C (MEF2C) gene promoter in Bos taurus cattle
A large number of Mef2c targets overlapped with genes down-regulated by Wnt16 (zeige WNT16 Proteine) and Mef2c itself was transcriptionally repressed by Wnt16 (zeige WNT16 Proteine) suggesting that Mef2c plays a role in Wnt16 (zeige WNT16 Proteine)-mediated transcriptional regulation.
results suggest that MEF2C haploinsufficiency leads to abnormal brain development, E/I imbalance, and neurobehavioral dysfunction, which may be mitigated by pharmacological intervention
MiR (zeige MLXIP Proteine)-204-5p inhibits myoblast differentiation by targeting MEF2C and ERRgamma (zeige ESRRG Proteine).
MEF2C protects B lymphopoiesis during stress by ensuring proper expression of genes that encode DNA repair and B-cell factors.
Enrichment of induced cardiomyocytes derived from mouse fibroblasts can be achieved by reprogramming with cardiac transcription factors, Gata4 (zeige GATA4 Proteine), MEF2c, Tbx5 (zeige TBX5 Proteine), and Hand2 (zeige HAND2 Proteine).
MEF2C is a novel target of miR (zeige MLXIP Proteine)-214-3p in myocardial hypertrophy, and enhancement of miR (zeige MLXIP Proteine)-214-3p expression may be protective against myocardial hypertrophy.
Results show that MEF2C interacts with the N-terminal pre-LIM (zeige PDLIM5 Proteine) region of nTRIP6 in proliferating myoblasts.
Immune challenge in mice lacking Mef2C in microglia results in an exaggerated microglial response and has an adverse effect on mice behaviour.
MEF2C is necessary for Mmp13 (zeige MMP13 Proteine) gene expression at the transcriptional level and participates in PTH (zeige PTH Proteine)-stimulated Mmp13 (zeige MMP13 Proteine) gene expression by increased binding to c-FOS at the AP-1 (zeige JUN Proteine) site in the Mmp13 (zeige MMP13 Proteine) promoter.
lf5 ChIP-seq revealed that Klf5 (zeige KLF5 Proteine) binding overlaps that of MyoD (zeige MYOD1 Proteine) and Mef2, and Klf5 (zeige KLF5 Proteine) physically associates with both MyoD (zeige MYOD1 Proteine) and Mef2. In addition, MyoD (zeige MYOD1 Proteine) recruitment was greatly reduced in the absence of Klf5 (zeige KLF5 Proteine). These results indicate that Klf5 (zeige KLF5 Proteine) is an essential regulator of skeletal muscle differentiation, acting in concert with myogenic transcription factors such as MyoD (zeige MYOD1 Proteine) and Mef2.
This locus encodes a member of the MADS box transcription enhancer factor 2 (MEF2) family of proteins, which play a role in myogenesis. The encoded protein, MEF2 polypeptide C, has both trans-activating and DNA binding activities. This protein may play a role in maintaining the differentiated state of muscle cells. Mutations and deletions at this locus have been associated with severe mental retardation, stereotypic movements, epilepsy, and cerebral malformation. Alternatively spliced transcript variants have been described.
myocyte-specific enhancer factor 2C
, myocyte enhancer factor 2C
, myocyte-specific enhancer factor 2C-like
, MADS box transcription enhancer factor 2, polypeptide C
, MADS box transcription enhancer factor 2, polypeptide C (myocyte enhancer factor 2C)
, Myocyte enhancer factor 2C protein
, myocyte enhancer factor 2c