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anti-Human MEF2C Antikörper:
anti-Mouse (Murine) MEF2C Antikörper:
anti-Rat (Rattus) MEF2C Antikörper:
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Cow (Bovine) Polyclonal MEF2C Primary Antibody für 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 für 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 für 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 (zeige MYEF2 Antikörper) 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 Antikörper) and Mef2c is not only required for MYH6 (zeige MYH6 Antikörper) expression but also essential for the early stages of heart development and survival
Mef2c and Mef2d (zeige MEF2D Antikörper) 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 (zeige WLS Antikörper) , ARHGAP1 (zeige ARHGAP1 Antikörper) , and 5' of MEF2C ( P- values < 8x10 - 5 ; false discovery rate (FDR) q-values < 0.01) that were much more strongly associated with BMD (zeige BEST1 Antikörper) compared to the GWAS SNPs.
Our analysis consistently identified significant sub-networks associated with the interacting transcription factors MEF2C and TWIST1 (zeige TWIST1 Antikörper), genes not previously associated with spontaneous preterm births , both of which regulate processes clearly relevant to birth timing.
Key role for miR (zeige MLXIP Antikörper)-214 in modulation of MEF2C-MYOCD (zeige MYOCD Antikörper)-LMOD1 (zeige LMOD1 Antikörper) 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 (zeige GATA4 Antikörper), cand TBX5 (zeige TBX5 Antikörper))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 (zeige PSG1 Antikörper) to activate human AQP1 (zeige AQP1 Antikörper) transcription by binding to its proximal promoter in human umbilical cord vein endothelial cells indicating that AQP1 (zeige AQP1 Antikörper) 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 (zeige MYEF2 Antikörper)) gene showed that MyoD (zeige MYOD1 Antikörper) and MEF2 (zeige MYEF2 Antikörper) 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 (zeige KLF5 Antikörper) binding overlaps that of MyoD (zeige MYOD1 Antikörper) and Mef2, and Klf5 (zeige KLF5 Antikörper) physically associates with both MyoD (zeige MYOD1 Antikörper) and Mef2. In addition, MyoD (zeige MYOD1 Antikörper) recruitment was greatly reduced in the absence of Klf5 (zeige KLF5 Antikörper). These results indicate that Klf5 (zeige KLF5 Antikörper) is an essential regulator of skeletal muscle differentiation, acting in concert with myogenic transcription factors such as MyoD (zeige MYOD1 Antikörper) and Mef2.
The authors show here that conditional embryonic deletion of Mef2c in cortical and hippocampal excitatory neurons (Emx1 (zeige EMX1 Antikörper)-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 (zeige FXN Antikörper) in the nervous system in mice also activates an iron/sphingolipid/PDK1 (zeige PDPK1 Antikörper)/Mef2 pathway, indicating that the mechanism is evolutionarily conserved.
Ca(2 (zeige CA2 Antikörper)+) signaling pathway increases Nr4a1 (zeige NR4A1 Antikörper) expression in MA-10 Leydig cells, at least in part, by enhancing the recruitment of coactivator most likely through the MEF2, AP1 (zeige JUN Antikörper), and CREB (zeige CREB1 Antikörper) transcription factors thus demonstrating an important interplay between the Ca(2 (zeige CA2 Antikörper)+) and cAMP pathways in regulating Nr4a1 (zeige NR4A1 Antikörper) expression.
HDAC5 (zeige HDAC5 Antikörper) emerges as a cellular conductor of MEF2C and M6a (zeige GPM6A Antikörper) activity and is regulated by miR (zeige MLXIP Antikörper)-124 and miR (zeige MLXIP Antikörper)-9 to control neurite development.
In cardiomyocytes exposed to biomechanical stimulation, FAK (zeige PTK2 Antikörper) accumulates in the nucleus, binds to and upregulates the transcriptional activity of MEF2c through an interaction with the FAK (zeige PTK2 Antikörper) focal adhesion targeting (FAT) domain.
In Fmr1 (zeige FMR1 Antikörper) KO neurons, Mdm2 (zeige MDM2 Antikörper) is hyperphosphorylated, nuclear localized basally, and unaffected by MEF2 activation, which our data suggest due to an enhanced interaction with Eukaryotic Elongation Factor (zeige TSFM Antikörper) 1alpha (EF1alpha), whose protein levels are elevated in Fmr1 (zeige FMR1 Antikörper) KO. Expression of a dephosphomimetic of Mdm2 (zeige MDM2 Antikörper) rescues PSD-95 (zeige DLG4 Antikörper) ubiquitination, degradation and synapse elimination in Fmr1 (zeige FMR1 Antikörper) KO neurons.
two MEF2 sites in the enhancer function cooperatively due to bridging of the MEF2C-bound sites by the SAP (zeige APCS Antikörper) domain-containing co-activator protein myocardin (zeige MYOCD Antikörper)
Our results elucidate the specific role of the transcription factors CREB (zeige CREB1 Antikörper), 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 (zeige FOXP2 Antikörper)-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