Ignet

Gene Information

Gene symbol: MEF2C

Gene name: myocyte enhancer factor 2C

HGNC ID: 6996

Related Genes

#	Gene Symbol	Number of hits
1	AGT	1 hits
2	CNBP	1 hits
3	CREBBP	1 hits
4	EP300	1 hits
5	GLI2	1 hits
6	HIF1A	1 hits
7	INS	1 hits
8	MAPK1	1 hits
9	MAPK14	1 hits
10	MEF2A	1 hits
11	MEF2D	1 hits
12	MIRN373	1 hits
13	MYEF2	1 hits
14	MYOD1	1 hits
15	NKX2-5	1 hits
16	NPPA	1 hits
17	NPPB	1 hits
18	PPARGC1A	1 hits
19	TBX5	1 hits

Related Sentences

#	PMID	Sentence
1	10748204	The MEF2A isoform is required for striated muscle-specific expression of the insulin-responsive GLUT4 glucose transporter.
2	10748204	Previously, we have demonstrated that an MEF2 consensus sequence located between -473/-464 in the human GLUT4 gene was essential for both tissue-specific and hormonal/metabolic regulation of GLUT4 expression (Thai, M.
3	10748204	To identify the specific MEF2 isoform(s) responsible for GLUT4 expression, we studied the pattern of expression of the MEF2 isoforms in insulin-sensitive tissues.
4	10748204	Both heart and skeletal muscle were found to express the MEF2A, MEF2C, and MEF2D isoforms but not MEF2B.
5	10748204	However, only the MEF2A protein was selectively down-regulated in insulin-deficient diabetes.
6	10748204	Electrophoretic mobility shift assays revealed that nuclear extracts from diabetic animals had reduced binding to the MEF2 binding site compared with extracts from control or insulin-treated animals.
7	10748204	However, addition of MEF2A to diabetic nuclear extracts fully restored binding activity to the MEF2 element.
8	10748204	These data strongly suggest that the MEF2A-MEF2D heterodimer is selectively decreased in insulin-deficient diabetes and is responsible for hormonally regulated expression of the GLUT4 gene.
9	15340086	MEF2C gamma- isoforms are much more robust than gamma+ forms in activating MEF2-responsive reporters in transfected fibroblasts despite indistinguishable expression levels, and they better synergize with MyoD in promoting myogenic conversion.
10	15340086	Cis effects of gamma on MEF2C DNA binding, dimerization, protein stability, or response to CaM or p38 mitogen-activated protein kinase signaling are not apparent, and the isolated gamma domain represses transcription when fused to Gal4.
11	15340086	Our findings indicate that gamma functions autonomously as a phosphoserine-dependent transrepressor to downregulate transactivation function of MEF2 factors and that alternative splicing and serine phosphorylation converge to provide complex combinatorial control of MEF2C activity.
12	15340086	MEF2C gamma- isoforms are much more robust than gamma+ forms in activating MEF2-responsive reporters in transfected fibroblasts despite indistinguishable expression levels, and they better synergize with MyoD in promoting myogenic conversion.
13	15340086	Cis effects of gamma on MEF2C DNA binding, dimerization, protein stability, or response to CaM or p38 mitogen-activated protein kinase signaling are not apparent, and the isolated gamma domain represses transcription when fused to Gal4.
14	15340086	Our findings indicate that gamma functions autonomously as a phosphoserine-dependent transrepressor to downregulate transactivation function of MEF2 factors and that alternative splicing and serine phosphorylation converge to provide complex combinatorial control of MEF2C activity.
15	15340086	MEF2C gamma- isoforms are much more robust than gamma+ forms in activating MEF2-responsive reporters in transfected fibroblasts despite indistinguishable expression levels, and they better synergize with MyoD in promoting myogenic conversion.
16	15340086	Cis effects of gamma on MEF2C DNA binding, dimerization, protein stability, or response to CaM or p38 mitogen-activated protein kinase signaling are not apparent, and the isolated gamma domain represses transcription when fused to Gal4.
17	15340086	Our findings indicate that gamma functions autonomously as a phosphoserine-dependent transrepressor to downregulate transactivation function of MEF2 factors and that alternative splicing and serine phosphorylation converge to provide complex combinatorial control of MEF2C activity.
18	15834131	Despite a location between the p38 MAPK docking domain and Thr phosphoacceptors of MEF2A and MEF2C, inclusion of beta does not influence responses of these factors to this signaling pathway.
19	18413674	We investigated the role of transcriptional coactivator p300 and its interaction with myocyte enhancer factor 2 (MEF2) in diabetes-induced cardiomyocyte hypertrophy.
20	18413674	Cardiomyocytes were analyzed with respect to their size. mRNA expression of p300, MEF2A, MEF2C, atrial natriuretic polypeptide (ANP), brain natriuretic polypeptide (BNP), angiotensinogen (ANG), cAMP-responsive element binding protein-binding protein (CBP), and protein analysis of MEF2 were done with or without p300 blockade.
21	18413674	The results were that cardiomyocytes, exposed to 25 mM glucose for 48 h, showed cellular hypertrophy and augmented mRNA expression of ANP, BNP, and ANG, molecular markers of cardiac hypertrophy.
22	18413674	Glucose caused a duration-dependent increase of mRNA and protein expression in MEF2A and MEF2C and transcriptional coactivator p300.
23	18413674	Similarly, ANP, BNP, and ANG mRNA expression was significantly higher in the hearts of diabetic rats compared with the controls, in association with increased p300, MEF2A, and MEF2C expression.
24	18413674	We investigated the role of transcriptional coactivator p300 and its interaction with myocyte enhancer factor 2 (MEF2) in diabetes-induced cardiomyocyte hypertrophy.
25	18413674	Cardiomyocytes were analyzed with respect to their size. mRNA expression of p300, MEF2A, MEF2C, atrial natriuretic polypeptide (ANP), brain natriuretic polypeptide (BNP), angiotensinogen (ANG), cAMP-responsive element binding protein-binding protein (CBP), and protein analysis of MEF2 were done with or without p300 blockade.
26	18413674	The results were that cardiomyocytes, exposed to 25 mM glucose for 48 h, showed cellular hypertrophy and augmented mRNA expression of ANP, BNP, and ANG, molecular markers of cardiac hypertrophy.
27	18413674	Glucose caused a duration-dependent increase of mRNA and protein expression in MEF2A and MEF2C and transcriptional coactivator p300.
28	18413674	Similarly, ANP, BNP, and ANG mRNA expression was significantly higher in the hearts of diabetic rats compared with the controls, in association with increased p300, MEF2A, and MEF2C expression.
29	18413674	We investigated the role of transcriptional coactivator p300 and its interaction with myocyte enhancer factor 2 (MEF2) in diabetes-induced cardiomyocyte hypertrophy.
30	18413674	Cardiomyocytes were analyzed with respect to their size. mRNA expression of p300, MEF2A, MEF2C, atrial natriuretic polypeptide (ANP), brain natriuretic polypeptide (BNP), angiotensinogen (ANG), cAMP-responsive element binding protein-binding protein (CBP), and protein analysis of MEF2 were done with or without p300 blockade.
31	18413674	The results were that cardiomyocytes, exposed to 25 mM glucose for 48 h, showed cellular hypertrophy and augmented mRNA expression of ANP, BNP, and ANG, molecular markers of cardiac hypertrophy.
32	18413674	Glucose caused a duration-dependent increase of mRNA and protein expression in MEF2A and MEF2C and transcriptional coactivator p300.
33	18413674	Similarly, ANP, BNP, and ANG mRNA expression was significantly higher in the hearts of diabetic rats compared with the controls, in association with increased p300, MEF2A, and MEF2C expression.
34	19065516	[Study of the 482G/A variation in PGC-1alpha gene domain MEF2C as possible mechanism of type 2 diabetes].
35	19720801	The microRNA signature in response to insulin reveals its implication in the transcriptional action of insulin in human skeletal muscle and the role of a sterol regulatory element-binding protein-1c/myocyte enhancer factor 2C pathway.
36	21704010	In vivo and in vitro studies have confirmed that three major subgroups of MAPK including ERK1/2, JNK, and p38, are specifically upregulated in cardiomyocyte hypertrophy during hyperglycemia.
37	21704010	Overexpression of miR-373 decreased the cell size, and also reduced the level of its target gene MEF2C, and miR-373 expression was regulated by p38.
38	23266826	Here, we demonstrate that the Hh effector, Gli2, regulates MyoD expression and associates with MyoD gene elements.
39	23266826	Finally, Gli2, MyoD, and MEF2C form a protein complex, which enhances MyoD activity on skeletal muscle-related promoters.
40	23619295	Using genome-wide expression profiling, we previously demonstrated that exposure to maternal diabetes resulted in dysregulation of the hypoxia-inducible factor 1 (HIF-1) pathway in the developing embryo.
41	23619295	We thus considered a possible link between HIF-1-regulated pathways and the development of congenital malformations.
42	23619295	HIF-1α heterozygous-null (Hif1a(+/-)) and wild type (Wt) littermate embryos were exposed to the intrauterine environment of a diabetic mother to analyze the frequency and morphology of congenital defects, and assess gene expression changes in Wt and Hif1a(+/-) embryos.
43	23619295	We also detected significant differences in the expression of key cardiac transcription factors, including Nkx2.5, Tbx5, and Mef2C, in diabetes-exposed Hif1a(+/-) embryonic hearts compared to Wt littermates.