Ignet

Gene Information

Gene symbol: NRF1

Gene name: nuclear respiratory factor 1

HGNC ID: 7996

Synonyms: EWG, ALPHA-PAL

Related Genes

#	Gene Symbol	Number of hits
1	ACOX1	1 hits
2	AKT1	1 hits
3	ATIC	1 hits
4	COX8A	1 hits
5	COX8B	1 hits
6	CREB1	1 hits
7	CS	1 hits
8	DNM3	1 hits
9	ESRRA	1 hits
10	FOXO3	1 hits
11	FXR1	1 hits
12	FXR2	1 hits
13	GABPA	1 hits
14	GTF3A	1 hits
15	HSPA1A	1 hits
16	IHG1	1 hits
17	INS	1 hits
18	MEF2A	1 hits
19	MFN1	1 hits
20	MFN2	1 hits
21	MYEF2	1 hits
22	NFE2L2	1 hits
23	NFYA	1 hits
24	NOX1	1 hits
25	PGC	1 hits
26	PPARA	1 hits
27	PPARG	1 hits
28	PPARGC1A	1 hits
29	PPARGC1B	1 hits
30	PRKAA2	1 hits
31	RAPGEF1	1 hits
32	SIRT1	1 hits
33	SLC2A4	1 hits
34	SOD2	1 hits
35	SP1	1 hits
36	SP3	1 hits
37	TFAM	1 hits
38	TP53	1 hits
39	UCP2	1 hits
40	UCP3	1 hits
41	USF1	1 hits
42	USF2	1 hits

Related Sentences

#	PMID	Sentence
1	12832613	Coordinated reduction of genes of oxidative metabolism in humans with insulin resistance and diabetes: Potential role of PGC1 and NRF1.
2	12832613	We demonstrate that insulin resistance and DM associate with reduced expression of multiple nuclear respiratory factor-1 (NRF-1)-dependent genes encoding key enzymes in oxidative metabolism and mitochondrial function.
3	12832613	Although NRF-1 expression is decreased only in diabetic subjects, expression of both PPAR gamma coactivator 1-alpha and-beta (PGC1-alpha/PPARGC1 and PGC1-beta/PERC), coactivators of NRF-1 and PPAR gamma-dependent transcription, is decreased in both diabetic subjects and family history-positive nondiabetic subjects.
4	12832613	Decreased PGC1 expression may be responsible for decreased expression of NRF-dependent genes, leading to the metabolic disturbances characteristic of insulin resistance and DM.
5	12832613	Coordinated reduction of genes of oxidative metabolism in humans with insulin resistance and diabetes: Potential role of PGC1 and NRF1.
6	12832613	We demonstrate that insulin resistance and DM associate with reduced expression of multiple nuclear respiratory factor-1 (NRF-1)-dependent genes encoding key enzymes in oxidative metabolism and mitochondrial function.
7	12832613	Although NRF-1 expression is decreased only in diabetic subjects, expression of both PPAR gamma coactivator 1-alpha and-beta (PGC1-alpha/PPARGC1 and PGC1-beta/PERC), coactivators of NRF-1 and PPAR gamma-dependent transcription, is decreased in both diabetic subjects and family history-positive nondiabetic subjects.
8	12832613	Decreased PGC1 expression may be responsible for decreased expression of NRF-dependent genes, leading to the metabolic disturbances characteristic of insulin resistance and DM.
9	12832613	Coordinated reduction of genes of oxidative metabolism in humans with insulin resistance and diabetes: Potential role of PGC1 and NRF1.
10	12832613	We demonstrate that insulin resistance and DM associate with reduced expression of multiple nuclear respiratory factor-1 (NRF-1)-dependent genes encoding key enzymes in oxidative metabolism and mitochondrial function.
11	12832613	Although NRF-1 expression is decreased only in diabetic subjects, expression of both PPAR gamma coactivator 1-alpha and-beta (PGC1-alpha/PPARGC1 and PGC1-beta/PERC), coactivators of NRF-1 and PPAR gamma-dependent transcription, is decreased in both diabetic subjects and family history-positive nondiabetic subjects.
12	12832613	Decreased PGC1 expression may be responsible for decreased expression of NRF-dependent genes, leading to the metabolic disturbances characteristic of insulin resistance and DM.
13	15294042	Such adaptations are largely the result of a coordinated genetic response that increases mitochondrial proteins, fatty acid oxidation enzymes and the exercise- and insulin-stimulated glucose transporter GLUT4, and shifts the contractile and regulatory proteins to their more efficient isoforms.
14	15294042	The PPAR gamma co-activator (PGC) family of proteins have been identified as the central family of transcriptional co-activators for induction of mitochondrial biogenesis.
15	15294042	PGC-1 alpha is activated by exercise, and is sufficient to produce the endurance phenotype through direct interactions with NRF-1 and PPAR alpha, and potentially NRF-2.
16	15479157	The roles of Sp1, Sp3, USF1/USF2 and NRF-1 in the regulation and three-dimensional structure of the Fragile X mental retardation gene promoter.
17	15479157	We had previously shown that in mouse brain extracts two of these sites are bound by USF1/USF2 (upstream stimulatory factors 1 and 2) heterodimers and NRF-1 (nuclear respiratory factor-1).
18	15479157	In the present study, we show that Sp1 (specificity protein 1) and Sp3 are also strong positive regulators of FMR1 promoter activity.
19	15479157	We also show that, like Sp1 and E-box-binding proteins such as USF1 and USF2, NRF-1 causes DNA bending, in this case producing a bend of 57 degrees towards the major groove.
20	15479157	We can reconcile these observations with the positive effect of Sp1 and Sp3 if protein-induced bending acts, at least in part, to bring together distally spaced factors important for transcription initiation.
21	15479157	The roles of Sp1, Sp3, USF1/USF2 and NRF-1 in the regulation and three-dimensional structure of the Fragile X mental retardation gene promoter.
22	15479157	We had previously shown that in mouse brain extracts two of these sites are bound by USF1/USF2 (upstream stimulatory factors 1 and 2) heterodimers and NRF-1 (nuclear respiratory factor-1).
23	15479157	In the present study, we show that Sp1 (specificity protein 1) and Sp3 are also strong positive regulators of FMR1 promoter activity.
24	15479157	We also show that, like Sp1 and E-box-binding proteins such as USF1 and USF2, NRF-1 causes DNA bending, in this case producing a bend of 57 degrees towards the major groove.
25	15479157	We can reconcile these observations with the positive effect of Sp1 and Sp3 if protein-induced bending acts, at least in part, to bring together distally spaced factors important for transcription initiation.
26	15479157	The roles of Sp1, Sp3, USF1/USF2 and NRF-1 in the regulation and three-dimensional structure of the Fragile X mental retardation gene promoter.
27	15479157	We had previously shown that in mouse brain extracts two of these sites are bound by USF1/USF2 (upstream stimulatory factors 1 and 2) heterodimers and NRF-1 (nuclear respiratory factor-1).
28	15479157	In the present study, we show that Sp1 (specificity protein 1) and Sp3 are also strong positive regulators of FMR1 promoter activity.
29	15479157	We also show that, like Sp1 and E-box-binding proteins such as USF1 and USF2, NRF-1 causes DNA bending, in this case producing a bend of 57 degrees towards the major groove.
30	15479157	We can reconcile these observations with the positive effect of Sp1 and Sp3 if protein-induced bending acts, at least in part, to bring together distally spaced factors important for transcription initiation.
31	16259958	Furthermore, expression of the mitochondrial biogenesis factors, nuclear respiratory factor-1 and mitochondrial transcription factor A, was significantly elevated in Hcy-treated cells.
32	16326070	Defective activation of the transcriptional coactivator PGC-1alpha may contribute to the gene expression pattern observed in diabetic and insulin-resistant skeletal muscle.
33	16326070	We studied PPARGC1A (PGC-1alpha), PPARGC1B (PGC-1beta), NRF1, and a variety of mitochondrial DNA (mtDNA) and nuclear-encoded mitochondrial genes critical for oxidative phosphorylation in soleus muscle biopsies obtained from six healthy men and women before and after 5 weeks of local muscle inactivity.
34	16326070	Further, although diabetes patients are typically inactive, our analysis indicates that local muscle inactivity may not be expected to contribute to the decreased NRF1 and PGC-1beta expression noted in insulin-resistant and Type 2 diabetes patients, suggesting these changes may be more disease specific.
35	16326070	Defective activation of the transcriptional coactivator PGC-1alpha may contribute to the gene expression pattern observed in diabetic and insulin-resistant skeletal muscle.
36	16326070	We studied PPARGC1A (PGC-1alpha), PPARGC1B (PGC-1beta), NRF1, and a variety of mitochondrial DNA (mtDNA) and nuclear-encoded mitochondrial genes critical for oxidative phosphorylation in soleus muscle biopsies obtained from six healthy men and women before and after 5 weeks of local muscle inactivity.
37	16326070	Further, although diabetes patients are typically inactive, our analysis indicates that local muscle inactivity may not be expected to contribute to the decreased NRF1 and PGC-1beta expression noted in insulin-resistant and Type 2 diabetes patients, suggesting these changes may be more disease specific.
38	16380484	Treatment with metformin and AICAR inhibited hyperglycemia-induced intracellular and mtROS production, stimulated AMP-activated protein kinase (AMPK) activity, and increased the expression of peroxisome proliferator-activated response-gamma coactivator-1alpha (PGC-1alpha) and manganese superoxide dismutase (MnSOD) mRNAs.
39	16380484	The dominant negative form of AMPKalpha1 diminished the effects of metformin and AICAR on these events, and an overexpression of PGC-1alpha completely blocked the hyperglycemia-induced mtROS production.
40	16380484	In addition, metformin and AICAR increased the mRNA expression of nuclear respiratory factor-1 and mitochondrial DNA transcription factor A (mtTFA) and stimulated the mitochondrial proliferation.
41	16644684	Insulin increased phosphorylation of Akt and Akt substrate of 160 kDa (AS160) in a dose-dependent manner, with comparable responses between groups.
42	16644684	Skeletal muscle mRNA expression of peroxisome proliferator-activated receptor (PPAR) gamma coactivator (PGC)-1alpha, PGC-1beta, PPARdelta, nuclear respiratory factor-1, and uncoupling protein-3 was comparable between first-degree relatives and control subjects.
43	16644684	In conclusion, the uncoupling of insulin action on Akt/AS160 signaling and glucose transport implicates defective GLUT4 trafficking as an early event in the pathogenesis of type 2 diabetes.
44	16886907	NF-Y, AP2, Nrf1 and Sp1 regulate the fragile X-related gene 2 (FXR2).
45	16886907	The protein product of this gene, FMRP (fragile X mental retardation protein), is thought to be involved in the translational regulation of mRNAs important for learning and memory.
46	16886907	Disruption of Fxr2 in mice produces learning and memory deficits, and Fmr1 and Fxr2 double-knockout mice have exaggerated impairments in certain neurobehavioral phenotypes relative to the single gene knockouts.
47	16886907	This has led to the suggestion that FMR1 and FXR2 functionally overlap and that increasing the expression of FXR2P may ameliorate the symptoms of an FMRP deficiency.
48	16886907	Interestingly, the region upstream of the FXR2 translation start site acts as a bidirectional promoter in rodents, driving transcription of an alternative transcript encoding the ABP (androgen-binding protein) [aABP (alternative ABP promoter)].
49	16886907	Gel electrophoretic mobility-shift assays, chromatin immunoprecipitation studies and co-transfection experiments with plasmids expressing these transcription factors or dominant-negative versions of these factors showed that NF-YA (nuclear transcription factor Yalpha), AP2 (activator protein 2), Nrf1 (nuclear respiratory factor/alpha-Pal) and Sp1 (specificity protein 1) all bind to the FXR2 promoter both in vitro and in vivo and positively regulate the FXR2 promoter.
50	16886907	NF-Y, AP2, Nrf1 and Sp1 regulate the fragile X-related gene 2 (FXR2).
51	16886907	The protein product of this gene, FMRP (fragile X mental retardation protein), is thought to be involved in the translational regulation of mRNAs important for learning and memory.
52	16886907	Disruption of Fxr2 in mice produces learning and memory deficits, and Fmr1 and Fxr2 double-knockout mice have exaggerated impairments in certain neurobehavioral phenotypes relative to the single gene knockouts.
53	16886907	This has led to the suggestion that FMR1 and FXR2 functionally overlap and that increasing the expression of FXR2P may ameliorate the symptoms of an FMRP deficiency.
54	16886907	Interestingly, the region upstream of the FXR2 translation start site acts as a bidirectional promoter in rodents, driving transcription of an alternative transcript encoding the ABP (androgen-binding protein) [aABP (alternative ABP promoter)].
55	16886907	Gel electrophoretic mobility-shift assays, chromatin immunoprecipitation studies and co-transfection experiments with plasmids expressing these transcription factors or dominant-negative versions of these factors showed that NF-YA (nuclear transcription factor Yalpha), AP2 (activator protein 2), Nrf1 (nuclear respiratory factor/alpha-Pal) and Sp1 (specificity protein 1) all bind to the FXR2 promoter both in vitro and in vivo and positively regulate the FXR2 promoter.
56	17609253	For this purpose, we studied the oxidative phosphorylation system (OXPHOS) enzymatic activities as well as the expression of genes involved in the coordinated regulation of both mitochondrial and nuclear genome (PGC-1alpha, NRF-1, NRF-2alpha, mtSSB, and TFAM) and mitochondrial function (COX-IV, COX-I, and beta-ATPase) in rat embryos from control and streptozotocin-induced diabetic mothers.
57	18074631	ERRalpha, NRF1 and NRF2 are key targets of the PGC1s in mitochondrial biogenesis.
58	18074631	This includes genes encoding mitochondrial proteins like SOD2, but also includes cytoplasmic proteins such as catalase and GPX1.
59	18222924	Nuclear respiratory factor 1 controls myocyte enhancer factor 2A transcription to provide a mechanism for coordinate expression of respiratory chain subunits.
60	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.
61	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.
62	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.
63	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.
64	18222924	NRF1 regulates MEF2A promoter-reporters according to overexpression, RNA interference underexpression, and promoter element mutation studies.
65	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.
66	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.
67	18222924	MEF2A also bound the MEF2A and PPARGC1A promoters in ChIP, placing it within a feedback loop with PGC1alpha in controlling NRF1 activity.
68	18222924	Our findings also account for the previously described indirect regulation by NRF1 of other MEF2 targets in muscle such as GLUT4.
69	18222924	Nuclear respiratory factor 1 controls myocyte enhancer factor 2A transcription to provide a mechanism for coordinate expression of respiratory chain subunits.
70	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.
71	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.
72	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.
73	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.
74	18222924	NRF1 regulates MEF2A promoter-reporters according to overexpression, RNA interference underexpression, and promoter element mutation studies.
75	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.
76	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.
77	18222924	MEF2A also bound the MEF2A and PPARGC1A promoters in ChIP, placing it within a feedback loop with PGC1alpha in controlling NRF1 activity.
78	18222924	Our findings also account for the previously described indirect regulation by NRF1 of other MEF2 targets in muscle such as GLUT4.
79	18222924	Nuclear respiratory factor 1 controls myocyte enhancer factor 2A transcription to provide a mechanism for coordinate expression of respiratory chain subunits.
80	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.
81	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.
82	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.
83	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.
84	18222924	NRF1 regulates MEF2A promoter-reporters according to overexpression, RNA interference underexpression, and promoter element mutation studies.
85	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.
86	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.
87	18222924	MEF2A also bound the MEF2A and PPARGC1A promoters in ChIP, placing it within a feedback loop with PGC1alpha in controlling NRF1 activity.
88	18222924	Our findings also account for the previously described indirect regulation by NRF1 of other MEF2 targets in muscle such as GLUT4.
89	18222924	Nuclear respiratory factor 1 controls myocyte enhancer factor 2A transcription to provide a mechanism for coordinate expression of respiratory chain subunits.
90	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.
91	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.
92	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.
93	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.
94	18222924	NRF1 regulates MEF2A promoter-reporters according to overexpression, RNA interference underexpression, and promoter element mutation studies.
95	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.
96	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.
97	18222924	MEF2A also bound the MEF2A and PPARGC1A promoters in ChIP, placing it within a feedback loop with PGC1alpha in controlling NRF1 activity.
98	18222924	Our findings also account for the previously described indirect regulation by NRF1 of other MEF2 targets in muscle such as GLUT4.
99	18222924	Nuclear respiratory factor 1 controls myocyte enhancer factor 2A transcription to provide a mechanism for coordinate expression of respiratory chain subunits.
100	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.
101	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.
102	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.
103	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.
104	18222924	NRF1 regulates MEF2A promoter-reporters according to overexpression, RNA interference underexpression, and promoter element mutation studies.
105	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.
106	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.
107	18222924	MEF2A also bound the MEF2A and PPARGC1A promoters in ChIP, placing it within a feedback loop with PGC1alpha in controlling NRF1 activity.
108	18222924	Our findings also account for the previously described indirect regulation by NRF1 of other MEF2 targets in muscle such as GLUT4.
109	18222924	Nuclear respiratory factor 1 controls myocyte enhancer factor 2A transcription to provide a mechanism for coordinate expression of respiratory chain subunits.
110	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.
111	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.
112	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.
113	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.
114	18222924	NRF1 regulates MEF2A promoter-reporters according to overexpression, RNA interference underexpression, and promoter element mutation studies.
115	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.
116	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.
117	18222924	MEF2A also bound the MEF2A and PPARGC1A promoters in ChIP, placing it within a feedback loop with PGC1alpha in controlling NRF1 activity.
118	18222924	Our findings also account for the previously described indirect regulation by NRF1 of other MEF2 targets in muscle such as GLUT4.
119	18222924	Nuclear respiratory factor 1 controls myocyte enhancer factor 2A transcription to provide a mechanism for coordinate expression of respiratory chain subunits.
120	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.
121	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.
122	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.
123	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.
124	18222924	NRF1 regulates MEF2A promoter-reporters according to overexpression, RNA interference underexpression, and promoter element mutation studies.
125	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.
126	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.
127	18222924	MEF2A also bound the MEF2A and PPARGC1A promoters in ChIP, placing it within a feedback loop with PGC1alpha in controlling NRF1 activity.
128	18222924	Our findings also account for the previously described indirect regulation by NRF1 of other MEF2 targets in muscle such as GLUT4.
129	18269170	ERRalpha, NRF1 and NRF2 are key targets of the PGC1s in mitochondrial biogenesis.
130	18269170	This includes genes encoding mitochondrial proteins like SOD2, but also includes cytoplasmic proteins like catalase and GPX1.
131	19429820	In CAECs resveratrol increased mitochondrial mass and mitochondrial DNA content, upregulated protein expression of electron transport chain constituents, and induced mitochondrial biogenesis factors (proliferator-activated receptor-coactivator-1alpha, nuclear respiratory factor-1, mitochondrial transcription factor A).
132	19429820	Sirtuin 1 (SIRT1) was induced, and endothelial nitric oxide (NO) synthase (eNOS) was upregulated in a SIRT1-dependent manner.
133	19429820	We propose that SIRT1, via a pathway that involves the upregulation of eNOS, induces mitochondrial biogenesis.
134	19477471	Increased expression of peroxisome proliferator-activated receptor-gamma coactivator-1alpha, nuclear respiratory factor-1, cytochrome c, cytochrome c oxidase-4, and glucose transporter 4 by KRG treatment indicates that activated AMPK also enhanced mitochondrial biogenesis and glucose utilization in skeletal muscle.
135	19477471	Although these findings suggest that KRG is likely to have beneficial effects on the amelioration of insulin resistance and the prevention of T2DM through the activation of AMPK, further clinical studies are required to evaluate the use of KRG as a supplementary agent for T2DM.
136	20369014	The identified transcription factors include members of the CREB, NRF1 and PPAR family, among others, and represent regulatory targets for further experimental analysis.
137	20533901	PGC-1alpha (peroxisome-proliferator-activated receptor gamma co-activator-1alpha) is a co-transcriptional regulation factor that induces mitochondrial biogenesis by activating different transcription factors, including nuclear respiratory factor 1 and nuclear respiratory factor 2, which activate mitochondrial transcription factor A.
138	20816089	Here, we show that SIRT1 forms a complex with FOXO3a and NRF1 on the SIRT6 promoter and positively regulates expression of SIRT6, which, in turn, negatively regulates glycolysis, triglyceride synthesis, and fat metabolism by deacetylating histone H3 lysine 9 in the promoter of many genes involved in these processes.
139	20981161	Low-Frequency Electroacupuncture Improves Insulin Sensitivity in Obese Diabetic Mice through Activation of SIRT1/PGC-1α in Skeletal Muscle.
140	20981161	EA was likewise observed to decrease free fatty acid levels in db/db mice; it increased protein expression in skeletal muscle Sirtuin 1 (SIRT1) and induced gene expression of peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), nuclear respiratory factor 1 (NRF1), and acyl-CoA oxidase (ACOX).
141	20981161	These results indicated that EA offers a beneficial effect on insulin resistance in obese and diabetic db/db mice, at least partly, via stimulation of SIRT1/PGC-1α, thus resulting in improved insulin signal.
142	21146886	Association between polymorphisms in RAPGEF1, TP53, NRF1 and type 2 diabetes in Chinese Han population.
143	21146886	The aim of the present study was to investigate the association between the polymorphisms of RAPGEF1, TP53 and NRF1 and the risk of type 2 diabetes in the Chinese Han population.
144	21146886	We genotyped rs11243444 (RAPGEF1), rs1042522 (TP53) and rs1882095 (NRF1) in a case-control study, including 273 type 2 diabetes and 247 healthy controls.
145	21146886	A significant association was found in a variant of TP53 (rs1042522, odd ratio (OR)=1.28, 95% confidence interval (CI)=1.00-1.64; P=0.046), whereas polymorphisms in RAPGEF1, NRF1 were not associated with the risk of type 2 diabetes.
146	21146886	Furthermore, a potential gene-gene interaction showed the odds of being affected with type 2 diabetes was 2.54 times greater in subjects with the TP53 (rs1042522) and RAPGEF1 (rs11243444) risk alleles than those without either (95% CI=1.34-4.81; P=0.004) and the NRF1 gene polymorphism reached significance when paired with TP53:(OR=3.87, 95% CI=1.87-8.40; P=0.0006).
147	21146886	We demonstrated that the polymorphism in TP53 (rs1042522) was associated with type 2 diabetes, and that potential interaction of TP53 (rs1042522) and RAPGEF1 (rs11243444), or NRF1 (rs1882095) increased the risk of type 2 diabetes.
148	21146886	Association between polymorphisms in RAPGEF1, TP53, NRF1 and type 2 diabetes in Chinese Han population.
149	21146886	The aim of the present study was to investigate the association between the polymorphisms of RAPGEF1, TP53 and NRF1 and the risk of type 2 diabetes in the Chinese Han population.
150	21146886	We genotyped rs11243444 (RAPGEF1), rs1042522 (TP53) and rs1882095 (NRF1) in a case-control study, including 273 type 2 diabetes and 247 healthy controls.
151	21146886	A significant association was found in a variant of TP53 (rs1042522, odd ratio (OR)=1.28, 95% confidence interval (CI)=1.00-1.64; P=0.046), whereas polymorphisms in RAPGEF1, NRF1 were not associated with the risk of type 2 diabetes.
152	21146886	Furthermore, a potential gene-gene interaction showed the odds of being affected with type 2 diabetes was 2.54 times greater in subjects with the TP53 (rs1042522) and RAPGEF1 (rs11243444) risk alleles than those without either (95% CI=1.34-4.81; P=0.004) and the NRF1 gene polymorphism reached significance when paired with TP53:(OR=3.87, 95% CI=1.87-8.40; P=0.0006).
153	21146886	We demonstrated that the polymorphism in TP53 (rs1042522) was associated with type 2 diabetes, and that potential interaction of TP53 (rs1042522) and RAPGEF1 (rs11243444), or NRF1 (rs1882095) increased the risk of type 2 diabetes.
154	21146886	Association between polymorphisms in RAPGEF1, TP53, NRF1 and type 2 diabetes in Chinese Han population.
155	21146886	The aim of the present study was to investigate the association between the polymorphisms of RAPGEF1, TP53 and NRF1 and the risk of type 2 diabetes in the Chinese Han population.
156	21146886	We genotyped rs11243444 (RAPGEF1), rs1042522 (TP53) and rs1882095 (NRF1) in a case-control study, including 273 type 2 diabetes and 247 healthy controls.
157	21146886	A significant association was found in a variant of TP53 (rs1042522, odd ratio (OR)=1.28, 95% confidence interval (CI)=1.00-1.64; P=0.046), whereas polymorphisms in RAPGEF1, NRF1 were not associated with the risk of type 2 diabetes.
158	21146886	Furthermore, a potential gene-gene interaction showed the odds of being affected with type 2 diabetes was 2.54 times greater in subjects with the TP53 (rs1042522) and RAPGEF1 (rs11243444) risk alleles than those without either (95% CI=1.34-4.81; P=0.004) and the NRF1 gene polymorphism reached significance when paired with TP53:(OR=3.87, 95% CI=1.87-8.40; P=0.0006).
159	21146886	We demonstrated that the polymorphism in TP53 (rs1042522) was associated with type 2 diabetes, and that potential interaction of TP53 (rs1042522) and RAPGEF1 (rs11243444), or NRF1 (rs1882095) increased the risk of type 2 diabetes.
160	21146886	Association between polymorphisms in RAPGEF1, TP53, NRF1 and type 2 diabetes in Chinese Han population.
161	21146886	The aim of the present study was to investigate the association between the polymorphisms of RAPGEF1, TP53 and NRF1 and the risk of type 2 diabetes in the Chinese Han population.
162	21146886	We genotyped rs11243444 (RAPGEF1), rs1042522 (TP53) and rs1882095 (NRF1) in a case-control study, including 273 type 2 diabetes and 247 healthy controls.
163	21146886	A significant association was found in a variant of TP53 (rs1042522, odd ratio (OR)=1.28, 95% confidence interval (CI)=1.00-1.64; P=0.046), whereas polymorphisms in RAPGEF1, NRF1 were not associated with the risk of type 2 diabetes.
164	21146886	Furthermore, a potential gene-gene interaction showed the odds of being affected with type 2 diabetes was 2.54 times greater in subjects with the TP53 (rs1042522) and RAPGEF1 (rs11243444) risk alleles than those without either (95% CI=1.34-4.81; P=0.004) and the NRF1 gene polymorphism reached significance when paired with TP53:(OR=3.87, 95% CI=1.87-8.40; P=0.0006).
165	21146886	We demonstrated that the polymorphism in TP53 (rs1042522) was associated with type 2 diabetes, and that potential interaction of TP53 (rs1042522) and RAPGEF1 (rs11243444), or NRF1 (rs1882095) increased the risk of type 2 diabetes.
166	21146886	Association between polymorphisms in RAPGEF1, TP53, NRF1 and type 2 diabetes in Chinese Han population.
167	21146886	The aim of the present study was to investigate the association between the polymorphisms of RAPGEF1, TP53 and NRF1 and the risk of type 2 diabetes in the Chinese Han population.
168	21146886	We genotyped rs11243444 (RAPGEF1), rs1042522 (TP53) and rs1882095 (NRF1) in a case-control study, including 273 type 2 diabetes and 247 healthy controls.
169	21146886	A significant association was found in a variant of TP53 (rs1042522, odd ratio (OR)=1.28, 95% confidence interval (CI)=1.00-1.64; P=0.046), whereas polymorphisms in RAPGEF1, NRF1 were not associated with the risk of type 2 diabetes.
170	21146886	Furthermore, a potential gene-gene interaction showed the odds of being affected with type 2 diabetes was 2.54 times greater in subjects with the TP53 (rs1042522) and RAPGEF1 (rs11243444) risk alleles than those without either (95% CI=1.34-4.81; P=0.004) and the NRF1 gene polymorphism reached significance when paired with TP53:(OR=3.87, 95% CI=1.87-8.40; P=0.0006).
171	21146886	We demonstrated that the polymorphism in TP53 (rs1042522) was associated with type 2 diabetes, and that potential interaction of TP53 (rs1042522) and RAPGEF1 (rs11243444), or NRF1 (rs1882095) increased the risk of type 2 diabetes.
172	21146886	Association between polymorphisms in RAPGEF1, TP53, NRF1 and type 2 diabetes in Chinese Han population.
173	21146886	The aim of the present study was to investigate the association between the polymorphisms of RAPGEF1, TP53 and NRF1 and the risk of type 2 diabetes in the Chinese Han population.
174	21146886	We genotyped rs11243444 (RAPGEF1), rs1042522 (TP53) and rs1882095 (NRF1) in a case-control study, including 273 type 2 diabetes and 247 healthy controls.
175	21146886	A significant association was found in a variant of TP53 (rs1042522, odd ratio (OR)=1.28, 95% confidence interval (CI)=1.00-1.64; P=0.046), whereas polymorphisms in RAPGEF1, NRF1 were not associated with the risk of type 2 diabetes.
176	21146886	Furthermore, a potential gene-gene interaction showed the odds of being affected with type 2 diabetes was 2.54 times greater in subjects with the TP53 (rs1042522) and RAPGEF1 (rs11243444) risk alleles than those without either (95% CI=1.34-4.81; P=0.004) and the NRF1 gene polymorphism reached significance when paired with TP53:(OR=3.87, 95% CI=1.87-8.40; P=0.0006).
177	21146886	We demonstrated that the polymorphism in TP53 (rs1042522) was associated with type 2 diabetes, and that potential interaction of TP53 (rs1042522) and RAPGEF1 (rs11243444), or NRF1 (rs1882095) increased the risk of type 2 diabetes.
178	21784897	IHG-1 promotes mitochondrial biogenesis by stabilizing PGC-1α.
179	21784897	IHG-1 overexpression increased mitochondrial mass and stabilized peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α).
180	21784897	Conversely, inhibition of IHG-1 expression decreased mitochondrial mass, downregulated mitochondrial proteins, and PGC-1α-regulated transcription factors, including nuclear respiratory factor 1 and mitochondrial transcription factor A (TFAM), and reduced activity of the TFAM promoter.
181	21784897	In the unilateral ureteral obstruction model, we observed higher PGC-1α protein expression and IHG-1 levels with fibrosis.
182	21784897	In a gene-expression database, we noted that renal biopsies of human diabetic nephropathy demonstrated higher expression of genes encoding key mitochondrial proteins, including cytochrome c and manganese superoxide dismutase, compared with control biopsies.
183	21784897	In summary, these data suggest that IHG-1 increases mitochondrial biogenesis by promoting PGC-1α-dependent processes, potentially contributing to the pathogenesis of renal fibrosis.
184	21911054	Damage of mtDNA, copy number, and biogenesis (PGC1, NRF1, TFAM) were analyzed in the retinas from streptozotocin-diabetic wild-type (WT) and MnSOD transgenic (Tg) mice.
185	21911054	Binding between TFAM and chaperone Hsp70 was quantified by coimmunoprecipitation.
186	21911054	The gene transcripts of PGC1, NRF1, and TFAM were increased, but mitochondrial accumulation of TFAM was significantly decreased, and the binding of Hsp70 and TFAM was subnormal compared to WT nondiabetic mice.
187	21911054	Damage of mtDNA, copy number, and biogenesis (PGC1, NRF1, TFAM) were analyzed in the retinas from streptozotocin-diabetic wild-type (WT) and MnSOD transgenic (Tg) mice.
188	21911054	Binding between TFAM and chaperone Hsp70 was quantified by coimmunoprecipitation.
189	21911054	The gene transcripts of PGC1, NRF1, and TFAM were increased, but mitochondrial accumulation of TFAM was significantly decreased, and the binding of Hsp70 and TFAM was subnormal compared to WT nondiabetic mice.
190	23073711	VSMCs subjected to hyperinsulinemia exhibited increased migration and proliferation, and this is paralleled by oxidative stress [increased NADPH oxidase activity, NADPH oxidase 1 mRNA expression, and reactive oxygen species (ROS) generation], alterations in mitochondrial physiology (membrane depolarization, decreased mitochondrial mass, and increased mitochondrial ROS), changes in mitochondrial biogenesis-related genes (mitofusin 1, mitofusin 2, dynamin-related protein 1, peroxisome proliferator-activated receptor gamma coactivator 1-alpha, peroxisome proliferator-activated receptor gamma coactivator 1-beta, nuclear respiratory factor 1, and uncoupling protein 2), and increased Akt phosphorylation.
191	23460046	Impaired mitochondrial biogenesis due to dysfunctional adiponectin-AMPK-PGC-1α signaling contributing to increased vulnerability in diabetic heart.
192	23460046	Whether adiponectin (APN), a potent cardioprotective molecule, regulates cardiac mitochondrial function has also not been previously investigated.
193	23460046	Moreover, mitochondrial biogenesis of ob/ob cardiomyocytes is significantly impaired, as evidenced by reduced Ppargc-1a/Nrf-1/Tfam mRNA levels, mitochondrial DNA content, ATP content, citrate synthase activity, complexes I/III/V activity, AMPK phosphorylation, and increased PGC-1α acetylation.
194	23460046	Since APN is an upstream activator of AMPK and APN plasma levels are significantly reduced in ob/ob mice, we further tested the hypothesis that reduced APN in ob/ob mice is causatively related to mitochondrial biogenesis impairment.
195	23700793	Apoptotic peaks, mitochondrial ultrastructure, ATP/ADP, mRNA levels of peroxisome proliferater activated receptor gamma coactivator-1 (PGC-1) and nucleus respiratory factor-1 (NRF-1) as well as insulin secretion were measured.
196	23700793	Palmitate could increase apoptotic peaks, decrease ATP/ADP ratio, enhance the expression of PGC-1 mRNA and NRF-1 mRNA, and decrease glucose stimulated insulin secretion (GSIS).
197	23700793	In contrast, PIO could decrease apoptotic peaks, restore partly ATP/ADP ratio, decrease the expression of PGC-1 mRNA and NRF-1 mRNA, and increase GSIS level.
198	23700793	These results demonstrate that PIO could ameliorate palmitate induced damage to mitochondrion ultrastructure and function and restore GSIS, accompanied by the modulation of PGC-1 and NRF-1 expression.
199	23700793	Apoptotic peaks, mitochondrial ultrastructure, ATP/ADP, mRNA levels of peroxisome proliferater activated receptor gamma coactivator-1 (PGC-1) and nucleus respiratory factor-1 (NRF-1) as well as insulin secretion were measured.
200	23700793	Palmitate could increase apoptotic peaks, decrease ATP/ADP ratio, enhance the expression of PGC-1 mRNA and NRF-1 mRNA, and decrease glucose stimulated insulin secretion (GSIS).
201	23700793	In contrast, PIO could decrease apoptotic peaks, restore partly ATP/ADP ratio, decrease the expression of PGC-1 mRNA and NRF-1 mRNA, and increase GSIS level.
202	23700793	These results demonstrate that PIO could ameliorate palmitate induced damage to mitochondrion ultrastructure and function and restore GSIS, accompanied by the modulation of PGC-1 and NRF-1 expression.
203	23700793	Apoptotic peaks, mitochondrial ultrastructure, ATP/ADP, mRNA levels of peroxisome proliferater activated receptor gamma coactivator-1 (PGC-1) and nucleus respiratory factor-1 (NRF-1) as well as insulin secretion were measured.
204	23700793	Palmitate could increase apoptotic peaks, decrease ATP/ADP ratio, enhance the expression of PGC-1 mRNA and NRF-1 mRNA, and decrease glucose stimulated insulin secretion (GSIS).
205	23700793	In contrast, PIO could decrease apoptotic peaks, restore partly ATP/ADP ratio, decrease the expression of PGC-1 mRNA and NRF-1 mRNA, and increase GSIS level.
206	23700793	These results demonstrate that PIO could ameliorate palmitate induced damage to mitochondrion ultrastructure and function and restore GSIS, accompanied by the modulation of PGC-1 and NRF-1 expression.
207	23700793	Apoptotic peaks, mitochondrial ultrastructure, ATP/ADP, mRNA levels of peroxisome proliferater activated receptor gamma coactivator-1 (PGC-1) and nucleus respiratory factor-1 (NRF-1) as well as insulin secretion were measured.
208	23700793	Palmitate could increase apoptotic peaks, decrease ATP/ADP ratio, enhance the expression of PGC-1 mRNA and NRF-1 mRNA, and decrease glucose stimulated insulin secretion (GSIS).
209	23700793	In contrast, PIO could decrease apoptotic peaks, restore partly ATP/ADP ratio, decrease the expression of PGC-1 mRNA and NRF-1 mRNA, and increase GSIS level.
210	23700793	These results demonstrate that PIO could ameliorate palmitate induced damage to mitochondrion ultrastructure and function and restore GSIS, accompanied by the modulation of PGC-1 and NRF-1 expression.
211	23936397	PGC-1α, a transcriptional coactivator, controls inflammation and mitochondrial gene expression in insulin-sensitive tissues following exercise intervention.
212	23936397	However, attributing such effects to PGC-1α is counfounded by exercise-induced fluctuations in blood glucose, insulin or bodyweight in diabetic patients.
213	23936397	Curiously, such an anti-inflammatory effect was also linked to attenuated expression of downstream transcription factors of PGC-1α such as NRF-1 and several respiratory genes.