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Mef2 (show MYEF2 Proteins) 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 (show TBX5 Proteins) and Mef2c is not only required for MYH6 (show MYH6 Proteins) expression but also essential for the early stages of heart development and survival
Mef2c and Mef2d (show MEF2D Proteins) are required for proper cardiac gene expression.
Mef2c is highly expressed in the retina where it modulates photoreceptor-specific gene expression
Study provides evidence that Mef2c cooperated with Sp1 (show PSG1 Proteins) to activate human AQP1 (show AQP1 Proteins) transcription by binding to its proximal promoter in human umbilical cord vein endothelial cells indicating that AQP1 (show AQP1 Proteins) is a direct target of Mef2c in regulating angiogenesis and vasculogenesis of endothelial cells.
Data show that microRNA miR (show MLXIP Proteins)-27a was essential for the shift of mesenchymal stem cells (MSCs) from osteogenic differentiation to adipogenic differentiation in osteoporosis by targeting myocyte enhancer factor 2 c (Mef2c).
New MEF2C mutation in MEF2C haploinsufficiency syndrome
Long non-coding RNA uc.167 influences cell proliferation, apoptosis and differentiation of P19 (show CDKN2D Proteins) cells by regulating Mef2c.
We describe the prenatal identification of 5q14.3 duplication, including MEF2C, in a monochorionic twin pregnancy with corpus callosum anomalies, confirmed by autopsy. To the best of our knowledge, this cerebral finding has been observed for the first time in 5q14.3 duplication patients, possibly widening the neurological picture of this scarcely known syndrome. A pathogenetic role of MEF2C overexpression in brain develop
The finding of a jugular pit (show IRF6 Proteins) in this patient facilitated the diagnosis, and he is, to our knowledge, the third case of jugular pit (show IRF6 Proteins) in association with 5q14.3 deletion incorporating the MEF2C locus.
MiR (show MLXIP Proteins)-135b-5p and MiR (show MLXIP Proteins)-499a-3p Promote Cell Proliferation and Migration in Atherosclerosis by Directly Targeting MEF2C
early B cell factor-1 (EBF1 (show EBF1 Proteins)) was identified as a co-regulator of gene expression with MEF2C.
Data show that high myocyte enhancer factor 2C (MEF2C) mRNA expression leads to overexpression of MEF2C protein, and these findings provide the rationale for therapeutic targeting of MEF2C transcriptional activation in acute myeloid leukemia (show BCL11A Proteins).
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
results identify a novel cooperation between MEF2 factors and NR2F2 (show NR2F2 Proteins) in the expression of the Akr1c14 gene
We conclude that ILK (show ILK Proteins) negatively and independently of PI3K regulated MEF2C phosphorylation activity and MCK (show CKM Proteins) mRNA expression in C2C12 cells
Data show that three transcriptional factors Gata4 (show GATA4 Proteins), Mef2c, and Tbx5 (show TBX5 Proteins) (abbreviated as GMT (show GAMT Proteins)) significantly improved murine embryonic stem cells (ESCs (show NR2E3 Proteins)) differentiated into cardiomyocytes.
MEF2C has a role in regulating outflow tract alignment and transcriptional control of Tdgf1 (show TDGF1 Proteins)
These findings uncover a novel role for Mef2c/d in coordinating the transcriptional network that promotes early B-cell development.
our data indicate that robust hypertrophic MEF2 activation in the heart in vivo requires a background of adiponectin (show ADIPOQ Proteins) signaling and that adiponectin (show ADIPOQ Proteins) signaling in primary isolated CM directly enhances MEF2 activity through activation of p38 MAPK (show MAPK14 Proteins)
SmarcA4 (show SMARCA4 Proteins) is required for synapse development and myocyte enhancer factor 2-mediated synapse remodeling
Our results identify novel target genes for MEF2 and define MEF2 as an important regulator of Leydig cell function and male reproduction.
this is a novel mechanism of H2S-mediated activation of MEF2C and induction of miR (show MLXIP Proteins)-133a and inhibition of hypertrophy in HHcy cardiomyocytes.
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