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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 (显示 MYEF2 ELISA试剂盒) 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 (显示 TBX5 ELISA试剂盒) and Mef2c is not only required for MYH6 (显示 MYH6 ELISA试剂盒) expression but also essential for the early stages of heart development and survival
Mef2c and Mef2d (显示 MEF2D ELISA试剂盒) 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 (显示 WLS ELISA试剂盒) , ARHGAP1 (显示 ARHGAP1 ELISA试剂盒) , and 5' of MEF2C ( P- values < 8x10 - 5 ; false discovery rate (FDR) q-values < 0.01) that were much more strongly associated with BMD (显示 BEST1 ELISA试剂盒) compared to the GWAS SNPs.
Our analysis consistently identified significant sub-networks associated with the interacting transcription factors MEF2C and TWIST1 (显示 TWIST1 ELISA试剂盒), genes not previously associated with spontaneous preterm births , both of which regulate processes clearly relevant to birth timing.
Key role for miR (显示 MLXIP ELISA试剂盒)-214 in modulation of MEF2C-MYOCD (显示 MYOCD ELISA试剂盒)-LMOD1 (显示 LMOD1 ELISA试剂盒) signaling.
Endothelial Mef2c regulates the endothelial actin cytoskeleton and inhibits smooth muscle cell migration into the intima.
The mRNA expressions of PPP3CB (显示 PPP3CB ELISA试剂盒) and MEF2C were significantly up-regulated, and CAMK1 (显示 CAMK1 ELISA试剂盒) and PPP3R1 (显示 PPP3R1 ELISA试剂盒) were significantly down-regulated in mitral regurgitation(MR) patients compared to normal subjects. Moreover, MR patients had significantly increased mRNA levels of PPP3CB (显示 PPP3CB ELISA试剂盒), MEF2C and PLCE1 (显示 PLCE1 ELISA试剂盒) compared to aortic valve disease patients
Findings suggest that a single introduction of the three cardiomyogenic transcription factor (GATA4 (显示 GATA4 ELISA试剂盒), cand TBX5 (显示 TBX5 ELISA试剂盒))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 (显示 PSG1 ELISA试剂盒) to activate human AQP1 (显示 AQP1 ELISA试剂盒) transcription by binding to its proximal promoter in human umbilical cord vein endothelial cells indicating that AQP1 (显示 AQP1 ELISA试剂盒) is a direct target of Mef2c in regulating angiogenesis and vasculogenesis of endothelial cells.
Deletion and mutation analyses of the promoter of pig myocyte enhancer factor 2 (MEF2 (显示 MYEF2 ELISA试剂盒)) gene showed that MyoD (显示 MYOD1 ELISA试剂盒) and MEF2 (显示 MYEF2 ELISA试剂盒) 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
Here, the authors show that loss of Fxn (显示 FXN ELISA试剂盒) in the nervous system in mice also activates an iron/sphingolipid/PDK1 (显示 PDPK1 ELISA试剂盒)/Mef2 pathway, indicating that the mechanism is evolutionarily conserved.
Ca(2 (显示 CA2 ELISA试剂盒)+) signaling pathway increases Nr4a1 (显示 NR4A1 ELISA试剂盒) expression in MA-10 Leydig cells, at least in part, by enhancing the recruitment of coactivator most likely through the MEF2, AP1 (显示 JUN ELISA试剂盒), and CREB (显示 CREB1 ELISA试剂盒) transcription factors thus demonstrating an important interplay between the Ca(2 (显示 CA2 ELISA试剂盒)+) and cAMP pathways in regulating Nr4a1 (显示 NR4A1 ELISA试剂盒) expression.
HDAC5 (显示 HDAC5 ELISA试剂盒) emerges as a cellular conductor of MEF2C and M6a (显示 GPM6A ELISA试剂盒) activity and is regulated by miR (显示 MLXIP ELISA试剂盒)-124 and miR (显示 MLXIP ELISA试剂盒)-9 to control neurite development.
In cardiomyocytes exposed to biomechanical stimulation, FAK (显示 PTK2 ELISA试剂盒) accumulates in the nucleus, binds to and upregulates the transcriptional activity of MEF2c through an interaction with the FAK (显示 PTK2 ELISA试剂盒) focal adhesion targeting (FAT) domain.
In Fmr1 (显示 FMR1 ELISA试剂盒) KO neurons, Mdm2 (显示 MDM2 ELISA试剂盒) is hyperphosphorylated, nuclear localized basally, and unaffected by MEF2 activation, which our data suggest due to an enhanced interaction with Eukaryotic Elongation Factor (显示 TSFM ELISA试剂盒) 1alpha (EF1alpha), whose protein levels are elevated in Fmr1 (显示 FMR1 ELISA试剂盒) KO. Expression of a dephosphomimetic of Mdm2 (显示 MDM2 ELISA试剂盒) rescues PSD-95 (显示 DLG4 ELISA试剂盒) ubiquitination, degradation and synapse elimination in Fmr1 (显示 FMR1 ELISA试剂盒) KO neurons.
two MEF2 sites in the enhancer function cooperatively due to bridging of the MEF2C-bound sites by the SAP (显示 APCS ELISA试剂盒) domain-containing co-activator protein myocardin (显示 MYOCD ELISA试剂盒)
Our results elucidate the specific role of the transcription factors CREB (显示 CREB1 ELISA试剂盒), 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 (显示 FOXP2 ELISA试剂盒)-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.
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