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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 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.
Mef2cbL contains an evolutionarily conserved domain derived from exonization of a fragment of intron 5, which confers the ability to induce ectopic muscle in mesoderm upon over-expression of the protein.
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 and Mef2c is not only required for MYH6 expression but also essential for the early stages of heart development and survival
Mef2c and Mef2d are required for proper cardiac gene expression.
We report heterozygous MEF2C loss-of-function as a possible cause of question mark ear associated with intellectual deficiency.
Novel MEF2C point mutations in Chinese patients with Rett (-like) syndrome or non-syndromic intellectual disability have been reported.
Fourteen patients were studied including four patients with mutations in the MEF2C gene revealed by exome sequencing
MEF2C SNPs rs1366594, rs12521522 and rs11951031 were examined in women for northern Mexico. No significant association was found with bone mineral density, although some trends were seen.
The previously identified major depressive disorder risk variant rs10514299 in TMEM161B-MEF2C predicts neuronal correlates of reward processing in an alcohol dependence phenotype, possibly explaining part of the shared pathophysiology and comorbidity between the disorders.
Targeting of LKB1 or SIK3 diminishes histone acetylation at MEF2C-bound enhancers and deprives leukemia cells of the output of this essential TF.
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-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 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, another cardiac core transcription factor that has been causally linked to Congenital heart disease (CHD).
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.
a MEF2C and CEBPA correlation in CML disease progression
Single nucleotide polymorphism in MEF2C gene is associated with major depressive disorder.
we identified novel associations in WLS , ARHGAP1 , and 5' of MEF2C ( P- values < 8x10 - 5 ; false discovery rate (FDR) q-values < 0.01) that were much more strongly associated with BMD compared to the GWAS SNPs.
Our analysis consistently identified significant sub-networks associated with the interacting transcription factors MEF2C and TWIST1, genes not previously associated with spontaneous preterm births , both of which regulate processes clearly relevant to birth timing.
Deletion and mutation analyses of the promoter of pig myocyte enhancer factor 2 (MEF2) gene showed that MyoD and MEF2 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.
The myocyte enhancer factor 2 family of MADS is highly expressed in cells of muscle lineage, where they have been proven to be important regulators of gene expression during the development of skeletal, cardiac and smooth muscle.
analysis of sequence and variations of the bovine myocyte enhancer factor 2C (MEF2C) gene promoter in Bos taurus cattle
Deletion of Mef2c in the early myocardial lineage using Nkx2-5(Cre) resulted in cardiac and vascular abnormalities that were indistinguishable from the defects in the global Mef2c knockout. In contrast, early deletion of Mef2c in the vascular endothelium using an Etv2::Cre line active prior to the onset of Mef2c expression resulted in viable offspring that were indistinguishable from wild type controls.
Mef2c degradation was mediated by Skp2 E3 ligase
Tbx1 regulates the Mef2c anterior heart field enhancer by inducing histone deacetylation.
This study demonstrated that using multidimensional integrative approaches, we identify MEF2C TF as promising therapeutic target for schizophrenia and other psychiatric disease associated with impaired cognition.
A large number of Mef2c targets overlapped with genes down-regulated by Wnt16 and Mef2c itself was transcriptionally repressed by Wnt16 suggesting that Mef2c plays a role in Wnt16-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-204-5p inhibits myoblast differentiation by targeting MEF2C and ERRgamma.
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, MEF2c, Tbx5, and Hand2.
MEF2C is a novel target of miR-214-3p in myocardial hypertrophy, and enhancement of miR-214-3p expression may be protective against myocardial hypertrophy.
Results show that MEF2C interacts with the N-terminal pre-LIM 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.
the expression and the phosphorylation of MEF2Calpha1 are critically required to sustain the adult myogenesis.
MEF2C is necessary for Mmp13 gene expression at the transcriptional level and participates in PTH-stimulated Mmp13 gene expression by increased binding to c-FOS at the AP-1 site in the Mmp13 promoter.
lf5 ChIP-seq revealed that Klf5 binding overlaps that of MyoD and Mef2, and Klf5 physically associates with both MyoD and Mef2. In addition, MyoD recruitment was greatly reduced in the absence of Klf5. These results indicate that Klf5 is an essential regulator of skeletal muscle differentiation, acting in concert with myogenic transcription factors such as MyoD and Mef2.
The authors show here that conditional embryonic deletion of Mef2c in cortical and hippocampal excitatory neurons (Emx1-lineage) produces a dramatic reduction in cortical network activity in vivo, due in part to a dramatic increase in inhibitory and a decrease in excitatory synaptic transmission. Perturbing MEF2C function in neocortex can produce autistic- and intellectual disability-like behaviors in mice.
Here, the authors show that loss of Fxn in the nervous system in mice also activates an iron/sphingolipid/PDK1/Mef2 pathway, indicating that the mechanism is evolutionarily conserved.
Ca(2+) signaling pathway increases Nr4a1 expression in MA-10 Leydig cells, at least in part, by enhancing the recruitment of coactivator most likely through the MEF2, AP1, and CREB transcription factors thus demonstrating an important interplay between the Ca(2+) and cAMP pathways in regulating Nr4a1 expression.
HDAC5 emerges as a cellular conductor of MEF2C and M6a activity and is regulated by miR-124 and miR-9 to control neurite development.
In cardiomyocytes exposed to biomechanical stimulation, FAK accumulates in the nucleus, binds to and upregulates the transcriptional activity of MEF2c through an interaction with the FAK focal adhesion targeting (FAT) domain.
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