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H cordata promotes the activation of HIF-1A (zeige HIF1A Proteine)-FOXO3 (zeige FOXO3 Proteine) and MEF2A pathways.
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 (zeige HDAC4 Proteine) and HDAC9 (zeige HDAC9 Proteine) inversely correlate with overall survival. The knock out of HDAC9 (zeige HDAC9 Proteine) 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/MI suggests that MEF2A may have a significant role in the pathogenesis of premature CAD/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 (zeige MAPK14 Proteine) is a key regulator of canonical Wnt (zeige WNT2 Proteine) signaling by promoting a phospho-dependent interaction between MEF2 and beta-catenin (zeige CTNNB1 Proteine) to enhance cooperative transcriptional activity and cell proliferation.
Mechanistically, MEF-2 (zeige MYEF2 Proteine) was recruited to the viral promoter (LTR, long terminal repeat) in the context of chromatin, and constituted Tax (zeige CNTN2 Proteine)/CREB (zeige CREB1 Proteine) transcriptional complex via direct binding to the HTLV-1 LTR.
Our results revealed a link and interaction between MEF2A and miR (zeige MLXIP Proteine)-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 (zeige SQSTM1 Proteine) lysosome destabilization leads to the disruption of MEF2A degradation as well as the dysregulation of its function
Both synapse silencing and elimination required de novo transcription, but only silencing required the activity-dependent transcription factors MEF2A/D.
Deficiency of AKT2 (zeige AKT2 Proteine) in myocardium results in diminished MEF2A abundance, which induced decreased size of cardiomyocytes. We additionally confirmed that EndoG (zeige ENDOG Proteine), which is also regulated by AKT2 (zeige AKT2 Proteine), is a suppressor of MEF2A in myocardium.
these data indicate that MEF2 (zeige MEF2C Proteine) and AP-1 (zeige JUN Proteine) confer antagonistic regulation of Hspb7 (zeige HSPB7 Proteine) gene expression in skeletal muscle, with implications for autophagy and muscle atrophy.
Nuclear HDAC4 (zeige HDAC5 Proteine) binds to chromatin as well as to MEF2A transcription factor, leading to histone deacetylation and altered neuronal gene expression. By using a Cdkl5 (zeige CDKL5 Proteine) knockout (Cdkl5 (zeige CDKL5 Proteine) -/Y) mouse model, we found that hypophosphorylated HDAC4 (zeige HDAC5 Proteine) 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 (zeige APOE Proteine) knockout mice, but has no effect on lipoprotein levels in plasma.
microRNAs encoded by the Gtl2-Dio3 (zeige DIO3 Proteine) noncoding RNA locus function downstream of the MEF2A
Our results indicated that exercise-induced CPT1b (zeige CPT1B Proteine) expression was at least in part mediated by HDAC5 (zeige HDAC5 Proteine)/MEF2A interaction.
Whereas MEF2A is absolutely required for proper myoblast differentiation, MEF2B (zeige MEF2B Proteine), -C, and -D were found to be dispensable for this process.
Mef2 (zeige MYEF2 Proteine) 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.
MEF2A is a positive regulator in skeletal muscle myoblast proliferation
polymorphisms in the bovine MEF2A gene and their effect on the MEF2A mRNA expression level in the longissimus dorsi muscle
These results show that NLK specifically regulates the MEF2A activity required for anterior formation in Xenopus 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.
MADS box transcription enhancer factor 2, polypeptide A (myocyte enhancer factor 2A)
, myocyte-specific enhancer factor 2A
, serum response factor-like protein 1
, myocyte enhancer factor 2a
, myocyte-specific enhancer factor 2a
, myocyte-specific enhancer factor 2A homolog
, serum response factor-like protein 2
, myocyte enhancer factor 2A
, myocyte-specific enhancer factor 2A-like