Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species
variable transposon epigenetic silencing underlies the variable mef2ca mutant bone phenotype, and could be a widespread mechanism of phenotypic variability in animals.
Mef2 (show MYEF2 ELISA Kits) 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 (show TBX5 ELISA Kits) and Mef2c is not only required for MYH6 (show MYH6 ELISA Kits) expression but also essential for the early stages of heart development and survival
Mef2c and Mef2d (show MEF2D ELISA Kits) are required for proper cardiac gene expression.
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 (show WLS ELISA Kits) , ARHGAP1 (show ARHGAP1 ELISA Kits) , and 5' of MEF2C ( P- values < 8x10 - 5 ; false discovery rate (FDR) q-values < 0.01) that were much more strongly associated with BMD (show BEST1 ELISA Kits) compared to the GWAS SNPs.
Our analysis consistently identified significant sub-networks associated with the interacting transcription factors MEF2C and TWIST1 (show TWIST1 ELISA Kits), genes not previously associated with spontaneous preterm births , both of which regulate processes clearly relevant to birth timing.
Key role for miR (show MLXIP ELISA Kits)-214 in modulation of MEF2C-MYOCD (show MYOCD ELISA Kits)-LMOD1 (show LMOD1 ELISA Kits) signaling.
Endothelial Mef2c regulates the endothelial actin cytoskeleton and inhibits smooth muscle cell migration into the intima.
The mRNA expressions of PPP3CB (show PPP3CB ELISA Kits) and MEF2C were significantly up-regulated, and CAMK1 (show CAMK1 ELISA Kits) and PPP3R1 (show PPP3R1 ELISA Kits) were significantly down-regulated in mitral regurgitation(MR) patients compared to normal subjects. Moreover, MR patients had significantly increased mRNA levels of PPP3CB (show PPP3CB ELISA Kits), MEF2C and PLCE1 (show PLCE1 ELISA Kits) compared to aortic valve disease patients
Findings suggest that a single introduction of the three cardiomyogenic transcription factor (GATA4 (show GATA4 ELISA Kits), cand TBX5 (show TBX5 ELISA Kits))genes using polyethyleneimine (PEI)-based transfection is sufficient for transdifferentiation of adipose-derived stem cells (hADSCs) towards the cardiomyogenic lineage.
Mef2c is highly expressed in the retina where it modulates photoreceptor-specific gene expression
Study provides evidence that Mef2c cooperated with Sp1 (show PSG1 ELISA Kits) to activate human AQP1 (show AQP1 ELISA Kits) transcription by binding to its proximal promoter in human umbilical cord vein endothelial cells indicating that AQP1 (show AQP1 ELISA Kits) is a direct target of Mef2c in regulating angiogenesis and vasculogenesis of endothelial cells.
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
In cardiomyocytes exposed to biomechanical stimulation, FAK (show PTK2 ELISA Kits) accumulates in the nucleus, binds to and upregulates the transcriptional activity of MEF2c through an interaction with the FAK (show PTK2 ELISA Kits) focal adhesion targeting (FAT) domain.
In Fmr1 (show FMR1 ELISA Kits) KO neurons, Mdm2 (show MDM2 ELISA Kits) is hyperphosphorylated, nuclear localized basally, and unaffected by MEF2 activation, which our data suggest due to an enhanced interaction with Eukaryotic Elongation Factor (show TSFM ELISA Kits) 1alpha (EF1alpha), whose protein levels are elevated in Fmr1 (show FMR1 ELISA Kits) KO. Expression of a dephosphomimetic of Mdm2 (show MDM2 ELISA Kits) rescues PSD-95 (show DLG4 ELISA Kits) ubiquitination, degradation and synapse elimination in Fmr1 (show FMR1 ELISA Kits) KO neurons.
two MEF2 sites in the enhancer function cooperatively due to bridging of the MEF2C-bound sites by the SAP (show APCS ELISA Kits) domain-containing co-activator protein myocardin (show MYOCD ELISA Kits)
Our results elucidate the specific role of the transcription factors CREB (show CREB1 ELISA Kits), SRF, and MEF2 in the depression and potentiation components of ODP in vivo, therefore better informing future attempts to find therapeutic targets for diseases where activity-dependent plasticity is disrupted.
that Foxp2 (show FOXP2 ELISA Kits)-Mef2C signaling is critical to corticostriatal circuit formation
Postnatal, postsynaptic deletion of Mef2c in a sparse population of L2/3 neurons suppressed development of excitatory synaptic connections from all local input pathways tested. In the same cell population, Mef2c deletion promoted the strength of excitatory inputs originating from contralateral neocortex. Both the synapse promoting and synapse suppressing effects of Mef2c deletion required normal whisking experience.
Critical role for MEF2C in the regulation of spine numbers with a dissociation of learning and memory, synaptic plasticity, and measures of autism-related behaviors in postnatal mouse brain.
Analysis of SOST (show SOST ELISA Kits) expression using large minigenes reveals the MEF2C binding site in the evolutionarily conserved region (ECR5) enhancer mediates forskolin, but not 1,25-dihydroxyvitamin D3 or TGFbeta1 (show TGFB1 ELISA Kits) responsiveness.
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