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Using a dominant-negative SmMef2 mutant, authors provide evidence that SmMef2 may regulate genes in the WNT (show WNT2 ELISA Kits) pathway.
The authors identify and characterize Mef2 (show MYEF2 ELISA Kits) 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 (show HDAC4 ELISA Kits) and HDAC9 (show HDAC9 ELISA Kits) inversely correlate with overall survival. The knock out of HDAC9 (show HDAC9 ELISA Kits) 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 (show CAD ELISA Kits)/MI suggests that MEF2A may have a significant role in the pathogenesis of premature CAD (show CAD ELISA Kits)/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 (show MAPK14 ELISA Kits) is a key regulator of canonical Wnt (show WNT2 ELISA Kits) signaling by promoting a phospho-dependent interaction between MEF2 and beta-catenin (show CTNNB1 ELISA Kits) to enhance cooperative transcriptional activity and cell proliferation.
Mechanistically, MEF-2 (show MYEF2 ELISA Kits) was recruited to the viral promoter (LTR, long terminal repeat) in the context of chromatin, and constituted Tax (show CNTN2 ELISA Kits)/CREB (show CREB1 ELISA Kits) transcriptional complex via direct binding to the HTLV-1 LTR.
Our results revealed a link and interaction between MEF2A and miR (show MLXIP ELISA Kits)-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 (show SQSTM1 ELISA Kits) 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 (show TGFB1 ELISA Kits) autoregulation circuitry.
Deficiency of AKT2 (show AKT2 ELISA Kits) in myocardium results in diminished MEF2A abundance, which induced decreased size of cardiomyocytes. We additionally confirmed that EndoG (show ENDOG ELISA Kits), which is also regulated by AKT2 (show AKT2 ELISA Kits), is a suppressor of MEF2A in myocardium.
these data indicate that MEF2 (show MEF2C ELISA Kits) and AP-1 (show JUN ELISA Kits) confer antagonistic regulation of Hspb7 (show HSPB7 ELISA Kits) gene expression in skeletal muscle, with implications for autophagy and muscle atrophy.
Nuclear HDAC4 (show HDAC5 ELISA Kits) binds to chromatin as well as to MEF2A transcription factor, leading to histone deacetylation and altered neuronal gene expression. By using a Cdkl5 (show CDKL5 ELISA Kits) knockout (Cdkl5 (show CDKL5 ELISA Kits) -/Y) mouse model, we found that hypophosphorylated HDAC4 (show HDAC5 ELISA Kits) 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 (show APOE ELISA Kits) knockout mice, but has no effect on lipoprotein levels in plasma.
microRNAs encoded by the Gtl2-Dio3 (show DIO3 ELISA Kits) noncoding RNA locus function downstream of the MEF2A
Our results indicated that exercise-induced CPT1b (show CPT1B ELISA Kits) expression was at least in part mediated by HDAC5 (show HDAC5 ELISA Kits)/MEF2A interaction.
Whereas MEF2A is absolutely required for proper myoblast differentiation, MEF2B (show MEF2B ELISA Kits), -C, and -D were found to be dispensable for this process.
A role for endogenous MEF2 (show MEF2C ELISA Kits) factors exclusively in hormone/Fsk/cAMP-induced Nr4a1 (show NR4A1 ELISA Kits) 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 (show MYEF2 ELISA Kits) 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