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Human Polyclonal MEF2A Primary Antibody for IHC - ABIN966555
Kato, Zhao, Morikawa, Sugiyama, Chakravortty, Koide, Yoshida, Tapping, Yang, Yokochi, Lee: Big mitogen-activated kinase regulates multiple members of the MEF2 protein family. in The Journal of biological chemistry 2000
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Human Polyclonal MEF2A Primary Antibody for IHC - ABIN966556
Zhao, New, Kravchenko, Kato, Gram, di Padova, Olson, Ulevitch, Han: Regulation of the MEF2 family of transcription factors by p38. in Molecular and cellular biology 1999
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Human Monoclonal MEF2A Primary Antibody for ELISA, WB - ABIN1724919
Guella, Rimoldi, Asselta, Ardissino, Francolini, Martinelli, Girelli, Peyvandi, Tubaro, Merlini, Mannucci, Duga: Association and functional analyses of MEF2A as a susceptibility gene for premature myocardial infarction and coronary artery disease. in Circulation. Cardiovascular genetics 2009
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Human Polyclonal MEF2A Primary Antibody for IHC, IHC (p) - ABIN4333438
Zehorai, Seger: Beta-like importins mediate the nuclear translocation of mitogen-activated protein kinases. in Molecular and cellular biology 2013
Human Polyclonal MEF2A Primary Antibody for IF, IHC - ABIN361950
Satoh, Ohnishi, Sato, Takeyama, Iemura, Natsume, Shibuya: Nemo-like kinase-myocyte enhancer factor 2A signaling regulates anterior formation in Xenopus development. in Molecular and cellular biology 2007
Using a dominant-negative SmMef2 mutant, authors provide evidence that SmMef2 may regulate genes in the WNT (显示 WNT2 抗体) pathway.
The authors identify and characterize Mef2 (显示 MYEF2 抗体) from the schistosome worm Schistosoma mansoni (SmMef2).
in leiomyosarcomas (LMS), this two-faced trait of MEF2 is relevant for tumor aggressiveness. Class IIa HDACs are overexpressed in 22% of LMS, where high levels of MEF2, HDAC4 (显示 HDAC4 抗体) and HDAC9 (显示 HDAC9 抗体) inversely correlate with overall survival. The knock out of HDAC9 (显示 HDAC9 抗体) suppresses the transformed phenotype of LMS cells, by restoring the transcriptional proficiency of some MEF2-target loci
The discovery of a novel MEF2A mutation in a Chinese family with premature CAD (显示 CAD 抗体)/MI suggests that MEF2A may have a significant role in the pathogenesis of premature CAD (显示 CAD 抗体)/MI.
The findings of this study are consistent with MEF2A deregulation conferring risk of formal thought disorder.
Variants in the 3'-UTR of MEF2A are associated with coronary artery disease in a Chinese Han population.
p38 MAPK (显示 MAPK14 抗体) is a key regulator of canonical Wnt (显示 WNT2 抗体) signaling by promoting a phospho-dependent interaction between MEF2 and beta-catenin (显示 CTNNB1 抗体) to enhance cooperative transcriptional activity and cell proliferation.
Mechanistically, MEF-2 (显示 MYEF2 抗体) was recruited to the viral promoter (LTR, long terminal repeat) in the context of chromatin, and constituted Tax (显示 CNTN2 抗体)/CREB (显示 CREB1 抗体) transcriptional complex via direct binding to the HTLV-1 LTR.
Our results revealed a link and interaction between MEF2A and miR (显示 MLXIP 抗体)-143 and suggested a potential mechanism for MEF2A to regulate H(2)O(2) -induced VSMC senescence.
six or seven amino acid deletions and synonymous mutations (147143G-->A)in exon 11 of the MEF2A gene may be correlated with susceptibility to coronary artery disease in the Chinese population
MEF2A is targeted to lysosomes for chaperone-mediated autophagy degradation; oxidative stress-induced (显示 SQSTM1 抗体) lysosome destabilization leads to the disruption of MEF2A degradation as well as the dysregulation of its function
MEF2 transcription factors promotes epithelial-mesenchymal transition and invasiveness of hepatocellular carcinoma through TGF-beta1 (显示 TGFB1 抗体) autoregulation circuitry.
Deficiency of AKT2 (显示 AKT2 抗体) in myocardium results in diminished MEF2A abundance, which induced decreased size of cardiomyocytes. We additionally confirmed that EndoG (显示 ENDOG 抗体), which is also regulated by AKT2 (显示 AKT2 抗体), is a suppressor of MEF2A in myocardium.
these data indicate that MEF2 (显示 MEF2C 抗体) and AP-1 (显示 JUN 抗体) confer antagonistic regulation of Hspb7 (显示 HSPB7 抗体) gene expression in skeletal muscle, with implications for autophagy and muscle atrophy.
Nuclear HDAC4 (显示 HDAC5 抗体) binds to chromatin as well as to MEF2A transcription factor, leading to histone deacetylation and altered neuronal gene expression. By using a Cdkl5 (显示 CDKL5 抗体) knockout (Cdkl5 (显示 CDKL5 抗体) -/Y) mouse model, we found that hypophosphorylated HDAC4 (显示 HDAC5 抗体) translocates to the nucleus of neural precursor cells, thereby reducing histone 3 acetylation.
Knockdown of MEF2A significantly reduced hyperglycemia-induced cardiac fibroblast proliferation and migration, myofibroblast differentiation, matrix metalloproteinase activities, and collagen production.
Lentivirus-mediated MEF 2A shRNA accelerates inflammation and atherosclerosis in APOE (显示 APOE 抗体) knockout mice, but has no effect on lipoprotein levels in plasma.
microRNAs encoded by the Gtl2-Dio3 (显示 DIO3 抗体) noncoding RNA locus function downstream of the MEF2A
Our results indicated that exercise-induced CPT1b (显示 CPT1B 抗体) expression was at least in part mediated by HDAC5 (显示 HDAC5 抗体)/MEF2A interaction.
Whereas MEF2A is absolutely required for proper myoblast differentiation, MEF2B (显示 MEF2B 抗体), -C, and -D were found to be dispensable for this process.
A role for endogenous MEF2 (显示 MEF2C 抗体) factors exclusively in hormone/Fsk/cAMP-induced Nr4a1 (显示 NR4A1 抗体) gene expression in mouse MA-10 Leydig cells.
These results show that NLK specifically regulates the MEF2A activity required for anterior formation in Xenopus development.
polymorphisms in the bovine MEF2A gene and their effect on the MEF2A mRNA expression level in the longissimus dorsi muscle
Mef2 (显示 MYEF2 抗体) controls skeletal muscle formation after terminal differentiation.
Results suggest that myocyte-specific enhancer factor 2A is essential for cardiac contractility
Results suggest that myocyte enhancer factor 2A is essential for zebrafish posterior somite development.
The protein encoded by this gene is a DNA-binding transcription factor that activates many muscle-specific, growth factor-induced, and stress-induced genes. The encoded protein can act as a homodimer or as a heterodimer and is involved in several cellular processes, including muscle development, neuronal differentiation, cell growth control, and apoptosis. Defects in this gene could be a cause of autosomal dominant coronary artery disease 1 with myocardial infarction (ADCAD1). Several transcript variants encoding different isoforms have been found for this gene.
myocyte-specific enhancer factor 2A
, myocyte-specific enhancer factor 2a
, myocyte enhancer factor 2A
, MADS box transcription enhancer factor 2, polypeptide A (myocyte enhancer factor 2A)
, myocyte-specific enhancer factor 2A-like
, myocyte-specific enhancer factor 2A homolog
, serum response factor-like protein 1
, serum response factor-like protein 2
, myocyte enhancer factor 2a