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抗Human MEF2C 抗体:
抗Mouse (Murine) MEF2C 抗体:
抗Rat (Rattus) MEF2C 抗体:
Cow (Bovine) Polyclonal MEF2C Primary Antibody for WB - ABIN2780048
Shen, Kamp, Gruendling, Higgins: A bifunctional O-GlcNAc transferase governs flagellar motility through anti-repression. in Genes & development 2006
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Human Polyclonal MEF2C Primary Antibody for ICC, IF - ABIN4333449
Wirrig, Hinton, Yutzey: Differential expression of cartilage and bone-related proteins in pediatric and adult diseased aortic valves. in Journal of molecular and cellular cardiology 2011
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Human Monoclonal MEF2C Primary Antibody for FACS, IHC - ABIN1098145
Xu, Cao, Wang, Xu, Chen, Xu: VEGF promotes the transcription of the human PRL-3 gene in HUVEC through transcription factor MEF2C. in PLoS ONE 2011
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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 抗体) 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 抗体) and Mef2c is not only required for MYH6 (显示 MYH6 抗体) expression but also essential for the early stages of heart development and survival
Mef2c and Mef2d (显示 MEF2D 抗体) 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 抗体) , ARHGAP1 (显示 ARHGAP1 抗体) , 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 抗体) compared to the GWAS SNPs.
Our analysis consistently identified significant sub-networks associated with the interacting transcription factors MEF2C and TWIST1 (显示 TWIST1 抗体), 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 抗体)-214 in modulation of MEF2C-MYOCD (显示 MYOCD 抗体)-LMOD1 (显示 LMOD1 抗体) signaling.
Endothelial Mef2c regulates the endothelial actin cytoskeleton and inhibits smooth muscle cell migration into the intima.
The mRNA expressions of PPP3CB and MEF2C were significantly up-regulated, and CAMK1 and PPP3R1 were significantly down-regulated in mitral regurgitation(MR) patients compared to normal subjects. Moreover, MR patients had significantly increased mRNA levels of PPP3CB, MEF2C and PLCE1 compared to aortic valve disease patients
Findings suggest that a single introduction of the three cardiomyogenic transcription factor (GATA4 (显示 GATA4 抗体), cand TBX5 (显示 TBX5 抗体))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 抗体) to activate human AQP1 (显示 AQP1 抗体) transcription by binding to its proximal promoter in human umbilical cord vein endothelial cells indicating that AQP1 (显示 AQP1 抗体) 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 抗体)) gene showed that MyoD (显示 MYOD1 抗体) and MEF2 (显示 MYEF2 抗体) 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
lf5 ChIP-seq revealed that Klf5 (显示 KLF5 抗体) binding overlaps that of MyoD (显示 MYOD1 抗体) and Mef2, and Klf5 (显示 KLF5 抗体) physically associates with both MyoD (显示 MYOD1 抗体) and Mef2. In addition, MyoD (显示 MYOD1 抗体) recruitment was greatly reduced in the absence of Klf5 (显示 KLF5 抗体). These results indicate that Klf5 (显示 KLF5 抗体) is an essential regulator of skeletal muscle differentiation, acting in concert with myogenic transcription factors such as MyoD (显示 MYOD1 抗体) and Mef2.
The authors show here that conditional embryonic deletion of Mef2c in cortical and hippocampal excitatory neurons (Emx1 (显示 EMX1 抗体)-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 (显示 FXN 抗体) in the nervous system in mice also activates an iron/sphingolipid/PDK1 (显示 PDPK1 抗体)/Mef2 pathway, indicating that the mechanism is evolutionarily conserved.
Ca(2 (显示 CA2 抗体)+) signaling pathway increases Nr4a1 (显示 NR4A1 抗体) 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 抗体), and CREB (显示 CREB1 抗体) transcription factors thus demonstrating an important interplay between the Ca(2 (显示 CA2 抗体)+) and cAMP pathways in regulating Nr4a1 (显示 NR4A1 抗体) expression.
HDAC5 (显示 HDAC5 抗体) emerges as a cellular conductor of MEF2C and M6a (显示 GPM6A 抗体) activity and is regulated by miR (显示 MLXIP 抗体)-124 and miR (显示 MLXIP 抗体)-9 to control neurite development.
In cardiomyocytes exposed to biomechanical stimulation, FAK (显示 PTK2 抗体) accumulates in the nucleus, binds to and upregulates the transcriptional activity of MEF2c through an interaction with the FAK (显示 PTK2 抗体) focal adhesion targeting (FAT) domain.
In Fmr1 (显示 FMR1 抗体) KO neurons, Mdm2 (显示 MDM2 抗体) 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 抗体) 1alpha (EF1alpha), whose protein levels are elevated in Fmr1 (显示 FMR1 抗体) KO. Expression of a dephosphomimetic of Mdm2 (显示 MDM2 抗体) rescues PSD-95 (显示 DLG4 抗体) ubiquitination, degradation and synapse elimination in Fmr1 (显示 FMR1 抗体) KO neurons.
two MEF2 sites in the enhancer function cooperatively due to bridging of the MEF2C-bound sites by the SAP (显示 APCS 抗体) domain-containing co-activator protein myocardin (显示 MYOCD 抗体)
Our results elucidate the specific role of the transcription factors CREB (显示 CREB1 抗体), 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 抗体)-Mef2C signaling is critical to corticostriatal circuit formation
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