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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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Human Monoclonal MEF2C Primary Antibody für FACS, ICC - ABIN4333450
Deczkowska, Matcovitch-Natan, Tsitsou-Kampeli, Ben-Hamo, Dvir-Szternfeld, Spinrad, Singer, David, Winter, Smith, Kertser, Baruch, Rosenzweig, Terem, Prinz, Villeda, Citri, Amit, Schwartz: Mef2C restrains microglial inflammatory response and is lost in brain ageing in an IFN-I-dependent manner. in Nature communications 2017
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.
Overexpression of MEF2C decreased miR (zeige MLXIP Antikörper)-448-induced VSMCs proliferation and migration.
MEF2C mRNA expression levels in AD subjects are significantly lower than those in control subjects and are correlated with disease severity.
The regulation mechanism of MIG6 (zeige ERRFI1 Antikörper) and suggests potential implications for the therapeutic strategies of gefitinib resistance through inhibiting MEF2C in hepatic cancer cells.
This study firstly associates MEF2C loss-of-function mutation with double outlet right ventricle in humans, which provides novel insight into the molecular pathogenesis of congenital heart diseases.
Combined with automated 2D nano-scale chromatography, Accumulated ion monitoring achieved subattomolar limits of detection of endogenous proteins in complex biological proteomes. This allowed quantitation of absolute abundance of the human transcription factor MEF2C at approximately 100 molecules/cell, and determination of its phosphorylation stoichiometry from as little as 1 mug of extracts isolated from 10,000 human ...
the mutation significantly diminished the synergistic activation between MEF2C and GATA4 (zeige GATA4 Antikörper), another cardiac core transcription factor that has been causally linked to Congenital heart disease (CHD (zeige CHDH Antikörper)).
MEF2C expression levels were significantly associated with or may even be predictive of the response to glucocorticoid treatment.
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
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
A large number of Mef2c targets overlapped with genes down-regulated by Wnt16 (zeige WNT16 Antikörper) and Mef2c itself was transcriptionally repressed by Wnt16 (zeige WNT16 Antikörper) suggesting that Mef2c plays a role in Wnt16 (zeige WNT16 Antikörper)-mediated transcriptional regulation.
results suggest that MEF2C haploinsufficiency leads to abnormal brain development, E/I imbalance, and neurobehavioral dysfunction, which may be mitigated by pharmacological intervention
MiR (zeige MLXIP Antikörper)-204-5p inhibits myoblast differentiation by targeting MEF2C and ERRgamma (zeige ESRRG Antikörper).
MEF2C protects B lymphopoiesis during stress by ensuring proper expression of genes that encode DNA repair and B-cell factors.
Enrichment of induced cardiomyocytes derived from mouse fibroblasts can be achieved by reprogramming with cardiac transcription factors, Gata4 (zeige GATA4 Antikörper), MEF2c, Tbx5 (zeige TBX5 Antikörper), and Hand2 (zeige HAND2 Antikörper).
MEF2C is a novel target of miR (zeige MLXIP Antikörper)-214-3p in myocardial hypertrophy, and enhancement of miR (zeige MLXIP Antikörper)-214-3p expression may be protective against myocardial hypertrophy.
Results show that MEF2C interacts with the N-terminal pre-LIM (zeige PDLIM5 Antikörper) region of nTRIP6 in proliferating myoblasts.
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 Antikörper) gene expression at the transcriptional level and participates in PTH (zeige PTH Antikörper)-stimulated Mmp13 (zeige MMP13 Antikörper) gene expression by increased binding to c-FOS at the AP-1 (zeige JUN Antikörper) site in the Mmp13 (zeige MMP13 Antikörper) promoter.
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.
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