Ignet

Gene Information

Gene symbol: MEF2A

Gene name: myocyte enhancer factor 2A

HGNC ID: 6993

Synonyms: RSRFC4, RSRFC9

Related Genes

#	Gene Symbol	Number of hits
1	AGT	1 hits
2	COX6A1	1 hits
3	COX8A	1 hits
4	CPT1B	1 hits
5	CREBBP	1 hits
6	EP300	1 hits
7	INS	1 hits
8	KLF15	1 hits
9	MAPK1	1 hits
10	MEF2C	1 hits
11	MEF2D	1 hits
12	MYEF2	1 hits
13	NDUFC2	1 hits
14	NPPA	1 hits
15	NPPB	1 hits
16	NRF1	1 hits
17	PPARA	1 hits
18	PPARGC1A	1 hits
19	RUNX1	1 hits
20	SLC2A4	1 hits
21	THADA	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	10748204	The MEF2A isoform is required for striated muscle-specific expression of the insulin-responsive GLUT4 glucose transporter.
10	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.
11	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.
12	10748204	Both heart and skeletal muscle were found to express the MEF2A, MEF2C, and MEF2D isoforms but not MEF2B.
13	10748204	However, only the MEF2A protein was selectively down-regulated in insulin-deficient diabetes.
14	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.
15	10748204	However, addition of MEF2A to diabetic nuclear extracts fully restored binding activity to the MEF2 element.
16	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.
17	10748204	The MEF2A isoform is required for striated muscle-specific expression of the insulin-responsive GLUT4 glucose transporter.
18	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.
19	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.
20	10748204	Both heart and skeletal muscle were found to express the MEF2A, MEF2C, and MEF2D isoforms but not MEF2B.
21	10748204	However, only the MEF2A protein was selectively down-regulated in insulin-deficient diabetes.
22	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.
23	10748204	However, addition of MEF2A to diabetic nuclear extracts fully restored binding activity to the MEF2 element.
24	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.
25	10748204	The MEF2A isoform is required for striated muscle-specific expression of the insulin-responsive GLUT4 glucose transporter.
26	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.
27	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.
28	10748204	Both heart and skeletal muscle were found to express the MEF2A, MEF2C, and MEF2D isoforms but not MEF2B.
29	10748204	However, only the MEF2A protein was selectively down-regulated in insulin-deficient diabetes.
30	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.
31	10748204	However, addition of MEF2A to diabetic nuclear extracts fully restored binding activity to the MEF2 element.
32	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.
33	11316766	The MEF2A and MEF2D isoforms are differentially regulated in muscle and adipose tissue during states of insulin deficiency.
34	11316766	Previously we have demonstrated that striated muscle GLUT4 gene expression decreased following streptozotocin-induced diabetes due to a loss of MEF2A transcription factor expression without any significant effect on the MEF2D isoform (Mora, S. and J.
35	11316766	However, addition of in vitro synthesized MEF2A to adipose nuclear extracts results in the formation of the expected MEF2/DNA complex.
36	11316766	Furthermore, in vivo overexpression of MEF2A selectively in adipose tissue did not affect GLUT4 or MEF2D expression and was not sufficient to prevent GLUT4 down-regulation that occurred in insulin-deficient states.
37	11316766	The MEF2A and MEF2D isoforms are differentially regulated in muscle and adipose tissue during states of insulin deficiency.
38	11316766	Previously we have demonstrated that striated muscle GLUT4 gene expression decreased following streptozotocin-induced diabetes due to a loss of MEF2A transcription factor expression without any significant effect on the MEF2D isoform (Mora, S. and J.
39	11316766	However, addition of in vitro synthesized MEF2A to adipose nuclear extracts results in the formation of the expected MEF2/DNA complex.
40	11316766	Furthermore, in vivo overexpression of MEF2A selectively in adipose tissue did not affect GLUT4 or MEF2D expression and was not sufficient to prevent GLUT4 down-regulation that occurred in insulin-deficient states.
41	11316766	The MEF2A and MEF2D isoforms are differentially regulated in muscle and adipose tissue during states of insulin deficiency.
42	11316766	Previously we have demonstrated that striated muscle GLUT4 gene expression decreased following streptozotocin-induced diabetes due to a loss of MEF2A transcription factor expression without any significant effect on the MEF2D isoform (Mora, S. and J.
43	11316766	However, addition of in vitro synthesized MEF2A to adipose nuclear extracts results in the formation of the expected MEF2/DNA complex.
44	11316766	Furthermore, in vivo overexpression of MEF2A selectively in adipose tissue did not affect GLUT4 or MEF2D expression and was not sufficient to prevent GLUT4 down-regulation that occurred in insulin-deficient states.
45	11316766	The MEF2A and MEF2D isoforms are differentially regulated in muscle and adipose tissue during states of insulin deficiency.
46	11316766	Previously we have demonstrated that striated muscle GLUT4 gene expression decreased following streptozotocin-induced diabetes due to a loss of MEF2A transcription factor expression without any significant effect on the MEF2D isoform (Mora, S. and J.
47	11316766	However, addition of in vitro synthesized MEF2A to adipose nuclear extracts results in the formation of the expected MEF2/DNA complex.
48	11316766	Furthermore, in vivo overexpression of MEF2A selectively in adipose tissue did not affect GLUT4 or MEF2D expression and was not sufficient to prevent GLUT4 down-regulation that occurred in insulin-deficient states.
49	12097321	The Krüppel-like factor KLF15 regulates the insulin-sensitive glucose transporter GLUT4.
50	12097321	GLUT4 is the main insulin-responsive glucose transporter and is expressed predominantly in muscle and adipose tissues.
51	12097321	This effect is specific to KLF15 as overexpression of two other Krüppel-like factors, KLF2/LKLF and KLF4/GKLF, did not induce GLUT4 expression.
52	12097321	In co-transfection assays, KLF15 and MEF2A, a known activator of GLUT4, synergistically activates the GLUT4 promoter.
53	15734836	Myocyte enhancer factor 2A (MEF2A) is a transcription factor that is involved in the regulation of GLUT4 expression.
54	15734836	GLUT4 protein was increased approximately 80%, GLUT4 mRNA was increased approximately 2.5-fold, MEF2A protein was increased twofold, and hexokinase II protein was increased approximately 2.5-fold 18 h after the last exercise bout.
55	15734836	The cyclosporin treatment completely inhibited calcineurin activity but did not affect the adaptive increases in GLUT4, MEF2A, or hexokinase expression.
56	15734836	Myocyte enhancer factor 2A (MEF2A) is a transcription factor that is involved in the regulation of GLUT4 expression.
57	15734836	GLUT4 protein was increased approximately 80%, GLUT4 mRNA was increased approximately 2.5-fold, MEF2A protein was increased twofold, and hexokinase II protein was increased approximately 2.5-fold 18 h after the last exercise bout.
58	15734836	The cyclosporin treatment completely inhibited calcineurin activity but did not affect the adaptive increases in GLUT4, MEF2A, or hexokinase expression.
59	15734836	Myocyte enhancer factor 2A (MEF2A) is a transcription factor that is involved in the regulation of GLUT4 expression.
60	15734836	GLUT4 protein was increased approximately 80%, GLUT4 mRNA was increased approximately 2.5-fold, MEF2A protein was increased twofold, and hexokinase II protein was increased approximately 2.5-fold 18 h after the last exercise bout.
61	15734836	The cyclosporin treatment completely inhibited calcineurin activity but did not affect the adaptive increases in GLUT4, MEF2A, or hexokinase expression.
62	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.
63	18222924	Nuclear respiratory factor 1 controls myocyte enhancer factor 2A transcription to provide a mechanism for coordinate expression of respiratory chain subunits.
64	18222924	Nuclear respiratory factors NRF1 and NRF2 regulate the expression of nuclear genes encoding heme biosynthetic enzymes, proteins required for mitochondrial genome transcription and protein import, and numerous respiratory chain subunits.
65	18222924	Only two of the nuclear-encoded respiratory chain subunits have evolutionarily conserved tissue-specific forms: the cytochrome c oxidase (COX) subunits VIa and VIIa heart/muscle (H) and ubiquitous (L) isoforms.
66	18222924	We used genome comparisons to conclude that the promoter regions of COX6A(H) and COX7A(H) lack NRF sites but have conserved myocyte enhancer factor 2 (MEF2) elements.
67	18222924	We show that MEF2A mRNA is induced with forced expression of NRF1 and that the MEF2A 5'-regulatory region contains an evolutionarily conserved canonical element that binds endogenous NRF1 in chromatin immunoprecipitation (ChIP) assays.
68	18222924	NRF1 regulates MEF2A promoter-reporters according to overexpression, RNA interference underexpression, and promoter element mutation studies.
69	18222924	As there are four mammalian MEF2 isotypes, we used an isoform-specific antibody in ChIP to confirm MEF2A binding to the COX6A(H) promoter.
70	18222924	These findings support a role for MEF2A as an intermediary in coordinating respiratory chain subunit expression in heart and muscle through a NRF1 --> MEF2A --> COX(H) transcriptional cascade.
71	18222924	MEF2A also bound the MEF2A and PPARGC1A promoters in ChIP, placing it within a feedback loop with PGC1alpha in controlling NRF1 activity.
72	18222924	Our findings also account for the previously described indirect regulation by NRF1 of other MEF2 targets in muscle such as GLUT4.
73	18222924	Nuclear respiratory factor 1 controls myocyte enhancer factor 2A transcription to provide a mechanism for coordinate expression of respiratory chain subunits.
74	18222924	Nuclear respiratory factors NRF1 and NRF2 regulate the expression of nuclear genes encoding heme biosynthetic enzymes, proteins required for mitochondrial genome transcription and protein import, and numerous respiratory chain subunits.
75	18222924	Only two of the nuclear-encoded respiratory chain subunits have evolutionarily conserved tissue-specific forms: the cytochrome c oxidase (COX) subunits VIa and VIIa heart/muscle (H) and ubiquitous (L) isoforms.
76	18222924	We used genome comparisons to conclude that the promoter regions of COX6A(H) and COX7A(H) lack NRF sites but have conserved myocyte enhancer factor 2 (MEF2) elements.
77	18222924	We show that MEF2A mRNA is induced with forced expression of NRF1 and that the MEF2A 5'-regulatory region contains an evolutionarily conserved canonical element that binds endogenous NRF1 in chromatin immunoprecipitation (ChIP) assays.
78	18222924	NRF1 regulates MEF2A promoter-reporters according to overexpression, RNA interference underexpression, and promoter element mutation studies.
79	18222924	As there are four mammalian MEF2 isotypes, we used an isoform-specific antibody in ChIP to confirm MEF2A binding to the COX6A(H) promoter.
80	18222924	These findings support a role for MEF2A as an intermediary in coordinating respiratory chain subunit expression in heart and muscle through a NRF1 --> MEF2A --> COX(H) transcriptional cascade.
81	18222924	MEF2A also bound the MEF2A and PPARGC1A promoters in ChIP, placing it within a feedback loop with PGC1alpha in controlling NRF1 activity.
82	18222924	Our findings also account for the previously described indirect regulation by NRF1 of other MEF2 targets in muscle such as GLUT4.
83	18222924	Nuclear respiratory factor 1 controls myocyte enhancer factor 2A transcription to provide a mechanism for coordinate expression of respiratory chain subunits.
84	18222924	Nuclear respiratory factors NRF1 and NRF2 regulate the expression of nuclear genes encoding heme biosynthetic enzymes, proteins required for mitochondrial genome transcription and protein import, and numerous respiratory chain subunits.
85	18222924	Only two of the nuclear-encoded respiratory chain subunits have evolutionarily conserved tissue-specific forms: the cytochrome c oxidase (COX) subunits VIa and VIIa heart/muscle (H) and ubiquitous (L) isoforms.
86	18222924	We used genome comparisons to conclude that the promoter regions of COX6A(H) and COX7A(H) lack NRF sites but have conserved myocyte enhancer factor 2 (MEF2) elements.
87	18222924	We show that MEF2A mRNA is induced with forced expression of NRF1 and that the MEF2A 5'-regulatory region contains an evolutionarily conserved canonical element that binds endogenous NRF1 in chromatin immunoprecipitation (ChIP) assays.
88	18222924	NRF1 regulates MEF2A promoter-reporters according to overexpression, RNA interference underexpression, and promoter element mutation studies.
89	18222924	As there are four mammalian MEF2 isotypes, we used an isoform-specific antibody in ChIP to confirm MEF2A binding to the COX6A(H) promoter.
90	18222924	These findings support a role for MEF2A as an intermediary in coordinating respiratory chain subunit expression in heart and muscle through a NRF1 --> MEF2A --> COX(H) transcriptional cascade.
91	18222924	MEF2A also bound the MEF2A and PPARGC1A promoters in ChIP, placing it within a feedback loop with PGC1alpha in controlling NRF1 activity.
92	18222924	Our findings also account for the previously described indirect regulation by NRF1 of other MEF2 targets in muscle such as GLUT4.
93	18222924	Nuclear respiratory factor 1 controls myocyte enhancer factor 2A transcription to provide a mechanism for coordinate expression of respiratory chain subunits.
94	18222924	Nuclear respiratory factors NRF1 and NRF2 regulate the expression of nuclear genes encoding heme biosynthetic enzymes, proteins required for mitochondrial genome transcription and protein import, and numerous respiratory chain subunits.
95	18222924	Only two of the nuclear-encoded respiratory chain subunits have evolutionarily conserved tissue-specific forms: the cytochrome c oxidase (COX) subunits VIa and VIIa heart/muscle (H) and ubiquitous (L) isoforms.
96	18222924	We used genome comparisons to conclude that the promoter regions of COX6A(H) and COX7A(H) lack NRF sites but have conserved myocyte enhancer factor 2 (MEF2) elements.
97	18222924	We show that MEF2A mRNA is induced with forced expression of NRF1 and that the MEF2A 5'-regulatory region contains an evolutionarily conserved canonical element that binds endogenous NRF1 in chromatin immunoprecipitation (ChIP) assays.
98	18222924	NRF1 regulates MEF2A promoter-reporters according to overexpression, RNA interference underexpression, and promoter element mutation studies.
99	18222924	As there are four mammalian MEF2 isotypes, we used an isoform-specific antibody in ChIP to confirm MEF2A binding to the COX6A(H) promoter.
100	18222924	These findings support a role for MEF2A as an intermediary in coordinating respiratory chain subunit expression in heart and muscle through a NRF1 --> MEF2A --> COX(H) transcriptional cascade.
101	18222924	MEF2A also bound the MEF2A and PPARGC1A promoters in ChIP, placing it within a feedback loop with PGC1alpha in controlling NRF1 activity.
102	18222924	Our findings also account for the previously described indirect regulation by NRF1 of other MEF2 targets in muscle such as GLUT4.
103	18222924	Nuclear respiratory factor 1 controls myocyte enhancer factor 2A transcription to provide a mechanism for coordinate expression of respiratory chain subunits.
104	18222924	Nuclear respiratory factors NRF1 and NRF2 regulate the expression of nuclear genes encoding heme biosynthetic enzymes, proteins required for mitochondrial genome transcription and protein import, and numerous respiratory chain subunits.
105	18222924	Only two of the nuclear-encoded respiratory chain subunits have evolutionarily conserved tissue-specific forms: the cytochrome c oxidase (COX) subunits VIa and VIIa heart/muscle (H) and ubiquitous (L) isoforms.
106	18222924	We used genome comparisons to conclude that the promoter regions of COX6A(H) and COX7A(H) lack NRF sites but have conserved myocyte enhancer factor 2 (MEF2) elements.
107	18222924	We show that MEF2A mRNA is induced with forced expression of NRF1 and that the MEF2A 5'-regulatory region contains an evolutionarily conserved canonical element that binds endogenous NRF1 in chromatin immunoprecipitation (ChIP) assays.
108	18222924	NRF1 regulates MEF2A promoter-reporters according to overexpression, RNA interference underexpression, and promoter element mutation studies.
109	18222924	As there are four mammalian MEF2 isotypes, we used an isoform-specific antibody in ChIP to confirm MEF2A binding to the COX6A(H) promoter.
110	18222924	These findings support a role for MEF2A as an intermediary in coordinating respiratory chain subunit expression in heart and muscle through a NRF1 --> MEF2A --> COX(H) transcriptional cascade.
111	18222924	MEF2A also bound the MEF2A and PPARGC1A promoters in ChIP, placing it within a feedback loop with PGC1alpha in controlling NRF1 activity.
112	18222924	Our findings also account for the previously described indirect regulation by NRF1 of other MEF2 targets in muscle such as GLUT4.
113	18222924	Nuclear respiratory factor 1 controls myocyte enhancer factor 2A transcription to provide a mechanism for coordinate expression of respiratory chain subunits.
114	18222924	Nuclear respiratory factors NRF1 and NRF2 regulate the expression of nuclear genes encoding heme biosynthetic enzymes, proteins required for mitochondrial genome transcription and protein import, and numerous respiratory chain subunits.
115	18222924	Only two of the nuclear-encoded respiratory chain subunits have evolutionarily conserved tissue-specific forms: the cytochrome c oxidase (COX) subunits VIa and VIIa heart/muscle (H) and ubiquitous (L) isoforms.
116	18222924	We used genome comparisons to conclude that the promoter regions of COX6A(H) and COX7A(H) lack NRF sites but have conserved myocyte enhancer factor 2 (MEF2) elements.
117	18222924	We show that MEF2A mRNA is induced with forced expression of NRF1 and that the MEF2A 5'-regulatory region contains an evolutionarily conserved canonical element that binds endogenous NRF1 in chromatin immunoprecipitation (ChIP) assays.
118	18222924	NRF1 regulates MEF2A promoter-reporters according to overexpression, RNA interference underexpression, and promoter element mutation studies.
119	18222924	As there are four mammalian MEF2 isotypes, we used an isoform-specific antibody in ChIP to confirm MEF2A binding to the COX6A(H) promoter.
120	18222924	These findings support a role for MEF2A as an intermediary in coordinating respiratory chain subunit expression in heart and muscle through a NRF1 --> MEF2A --> COX(H) transcriptional cascade.
121	18222924	MEF2A also bound the MEF2A and PPARGC1A promoters in ChIP, placing it within a feedback loop with PGC1alpha in controlling NRF1 activity.
122	18222924	Our findings also account for the previously described indirect regulation by NRF1 of other MEF2 targets in muscle such as GLUT4.
123	18413674	We investigated the role of transcriptional coactivator p300 and its interaction with myocyte enhancer factor 2 (MEF2) in diabetes-induced cardiomyocyte hypertrophy.
124	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.
125	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.
126	18413674	Glucose caused a duration-dependent increase of mRNA and protein expression in MEF2A and MEF2C and transcriptional coactivator p300.
127	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.
128	18413674	We investigated the role of transcriptional coactivator p300 and its interaction with myocyte enhancer factor 2 (MEF2) in diabetes-induced cardiomyocyte hypertrophy.
129	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.
130	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.
131	18413674	Glucose caused a duration-dependent increase of mRNA and protein expression in MEF2A and MEF2C and transcriptional coactivator p300.
132	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.
133	18413674	We investigated the role of transcriptional coactivator p300 and its interaction with myocyte enhancer factor 2 (MEF2) in diabetes-induced cardiomyocyte hypertrophy.
134	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.
135	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.
136	18413674	Glucose caused a duration-dependent increase of mRNA and protein expression in MEF2A and MEF2C and transcriptional coactivator p300.
137	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.
138	19233164	CPT-1B is induced by the transcription factors peroxisome proliferator activated receptor-alpha (PPAR-alpha) and PPAR-gamma-coactivator 1alpha (PGC1alpha) and repressed by upstream stimulatory factor-2 (USF-2).
139	19233164	We therefore hypothesized that metoprolol represses CPT-1B by increasing USF-2-mediated repression of PGC1alpha.
140	19233164	After termination, the expression of CPT-1 isoforms, PPAR-alpha, PGC1alpha USF-1 and USF-2, as well as downstream targets were measured.
141	19233164	Binding of PPAR-alpha, PGC1alpha and USF-2 to PGC1alpha was measured using coimmunoprecipitation.
142	19233164	The occupation of PPAR-alpha and MEF-2A consensus sites in the CPT-1B promoter was measured using chromatin immunoprecipitation assays.
143	19233164	The expression of USF-2 was increased by metoprolol in both control and diabetic hearts, but the association of USF-2 with PGC1alpha was increased by metoprolol only in diabetic hearts.
144	19233164	Metoprolol prevented the increase in PGC1alpha occupation of the CPT-1B promoter region observed in the diabetic heart without affecting PPAR-alpha occupation.
145	19233164	Metoprolol decreases CPT-1B expression by decreasing PGC1alpha-mediated coactivation of PPAR-alpha and MEF-2A.
146	19233164	This is associated with increased PGC1alpha/ USF-2 binding, suggesting that USF-2 mediates the metoprolol-induced repression of PGC1alpha.
147	19233164	CPT-1B is induced by the transcription factors peroxisome proliferator activated receptor-alpha (PPAR-alpha) and PPAR-gamma-coactivator 1alpha (PGC1alpha) and repressed by upstream stimulatory factor-2 (USF-2).
148	19233164	We therefore hypothesized that metoprolol represses CPT-1B by increasing USF-2-mediated repression of PGC1alpha.
149	19233164	After termination, the expression of CPT-1 isoforms, PPAR-alpha, PGC1alpha USF-1 and USF-2, as well as downstream targets were measured.
150	19233164	Binding of PPAR-alpha, PGC1alpha and USF-2 to PGC1alpha was measured using coimmunoprecipitation.
151	19233164	The occupation of PPAR-alpha and MEF-2A consensus sites in the CPT-1B promoter was measured using chromatin immunoprecipitation assays.
152	19233164	The expression of USF-2 was increased by metoprolol in both control and diabetic hearts, but the association of USF-2 with PGC1alpha was increased by metoprolol only in diabetic hearts.
153	19233164	Metoprolol prevented the increase in PGC1alpha occupation of the CPT-1B promoter region observed in the diabetic heart without affecting PPAR-alpha occupation.
154	19233164	Metoprolol decreases CPT-1B expression by decreasing PGC1alpha-mediated coactivation of PPAR-alpha and MEF-2A.
155	19233164	This is associated with increased PGC1alpha/ USF-2 binding, suggesting that USF-2 mediates the metoprolol-induced repression of PGC1alpha.
156	23028138	We found differential DNA methylation of genes in biological pathways including mitogen-activated protein kinase (MAPK), insulin, and calcium signaling (P ≤ 0.007) and of individual genes with known function in muscle, including MAPK1, MYO18B, HOXC6, and the AMP-activated protein kinase subunit PRKAB1 in skeletal muscle of FH(+) compared with FH(-) men.
157	23028138	DNA methylation of genes in retinol metabolism and calcium signaling pathways (P < 3 × 10(-6)) and with known functions in muscle and T2D including MEF2A, RUNX1, NDUFC2, and THADA decreased after exercise.
158	23028138	In addition, both expression and methylation of several genes, i.e., ADIPOR1, BDKRB2, and TRIB1, changed after exercise.