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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 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 (zeige TBX5 ELISA Kits) and Mef2c is not only required for MYH6 (zeige MYH6 ELISA Kits) expression but also essential for the early stages of heart development and survival
Mef2c and Mef2d (zeige MEF2D ELISA Kits) are required for proper cardiac gene expression.
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 (zeige WLS ELISA Kits) , ARHGAP1 (zeige 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 (zeige BEST1 ELISA Kits) compared to the GWAS SNPs.
Our analysis consistently identified significant sub-networks associated with the interacting transcription factors MEF2C and TWIST1 (zeige 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 (zeige MLXIP ELISA Kits)-214 in modulation of MEF2C-MYOCD (zeige MYOCD ELISA Kits)-LMOD1 (zeige 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 (zeige PPP3CB ELISA Kits) and MEF2C were significantly up-regulated, and CAMK1 (zeige CAMK1 ELISA Kits) and PPP3R1 (zeige 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 (zeige PPP3CB ELISA Kits), MEF2C and PLCE1 (zeige PLCE1 ELISA Kits) compared to aortic valve disease patients
Findings suggest that a single introduction of the three cardiomyogenic transcription factor (GATA4 (zeige GATA4 ELISA Kits), cand TBX5 (zeige TBX5 ELISA Kits))genes using polyethyleneimine (PEI)-based transfection is sufficient for transdifferentiation of adipose-derived stem cells (hADSCs) towards the cardiomyogenic lineage.
Deletion and mutation analyses of the promoter of pig myocyte enhancer factor 2 (MEF2 (zeige MYEF2 ELISA Kits)) gene showed that MyoD (zeige MYOD1 ELISA Kits) and MEF2 (zeige MYEF2 ELISA Kits) 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
Immune challenge in mice lacking Mef2C in microglia results in an exaggerated microglial response and has an adverse effect on mice behaviour.
MEF2C is necessary for Mmp13 (zeige MMP13 ELISA Kits) gene expression at the transcriptional level and participates in PTH (zeige PTH ELISA Kits)-stimulated Mmp13 (zeige MMP13 ELISA Kits) gene expression by increased binding to c-FOS at the AP-1 (zeige JUN ELISA Kits) site in the Mmp13 (zeige MMP13 ELISA Kits) promoter.
lf5 ChIP-seq revealed that Klf5 (zeige KLF5 ELISA Kits) binding overlaps that of MyoD (zeige MYOD1 ELISA Kits) and Mef2, and Klf5 (zeige KLF5 ELISA Kits) physically associates with both MyoD (zeige MYOD1 ELISA Kits) and Mef2. In addition, MyoD (zeige MYOD1 ELISA Kits) recruitment was greatly reduced in the absence of Klf5 (zeige KLF5 ELISA Kits). These results indicate that Klf5 (zeige KLF5 ELISA Kits) is an essential regulator of skeletal muscle differentiation, acting in concert with myogenic transcription factors such as MyoD (zeige MYOD1 ELISA Kits) 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 (zeige FXN ELISA Kits) in the nervous system in mice also activates an iron/sphingolipid/PDK1 (zeige PDPK1 ELISA Kits)/Mef2 pathway, indicating that the mechanism is evolutionarily conserved.
Ca(2 (zeige CA2 ELISA Kits)+) signaling pathway increases Nr4a1 (zeige NR4A1 ELISA Kits) expression in MA-10 Leydig cells, at least in part, by enhancing the recruitment of coactivator most likely through the MEF2, AP1 (zeige JUN ELISA Kits), and CREB (zeige CREB1 ELISA Kits) transcription factors thus demonstrating an important interplay between the Ca(2 (zeige CA2 ELISA Kits)+) and cAMP pathways in regulating Nr4a1 (zeige NR4A1 ELISA Kits) expression.
HDAC5 (zeige HDAC5 ELISA Kits) emerges as a cellular conductor of MEF2C and M6a (zeige GPM6A ELISA Kits) activity and is regulated by miR (zeige MLXIP ELISA Kits)-124 and miR (zeige MLXIP ELISA Kits)-9 to control neurite development.
In cardiomyocytes exposed to biomechanical stimulation, FAK (zeige PTK2 ELISA Kits) accumulates in the nucleus, binds to and upregulates the transcriptional activity of MEF2c through an interaction with the FAK (zeige PTK2 ELISA Kits) focal adhesion targeting (FAT) domain.
In Fmr1 (zeige FMR1 ELISA Kits) KO neurons, Mdm2 (zeige 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 (zeige TSFM ELISA Kits) 1alpha (EF1alpha), whose protein levels are elevated in Fmr1 (zeige FMR1 ELISA Kits) KO. Expression of a dephosphomimetic of Mdm2 (zeige MDM2 ELISA Kits) rescues PSD-95 (zeige DLG4 ELISA Kits) ubiquitination, degradation and synapse elimination in Fmr1 (zeige FMR1 ELISA Kits) KO neurons.
two MEF2 sites in the enhancer function cooperatively due to bridging of the MEF2C-bound sites by the SAP (zeige APCS ELISA Kits) domain-containing co-activator protein myocardin (zeige MYOCD ELISA Kits)
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