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1 NRF scores and mean national food prices were calculated
2 NRF's and YY1 were also detected in the paternal promote
3 NRF-1 and NRF-2 act additively while NRF-2 synergizes wi
4 NRF-1 and Sp1 are known to bind and stimulate the active
5 NRF-1 binding sites on Grin1 and Grin2b genes are also h
6 NRF-1 expression and growth were restored by exogenous o
7 NRF-1 functionally regulates mediators of energy consump
8 NRF-1 gene silencing blocked aerobic succinate oxidation
9 NRF-1 gene silencing produced 1:1 knockdown of Tfam expr
10 NRF-1 regulates mediators of neuronal activity and energ
11 NRF-1 transcriptionally regulates Na(+)/K(+)-ATPase subu
12 NRF-1-Tfam binding was augmented under pro-oxidant condi
13 NRF-2 is of special significance because it co-regulates
14 NRF-5 is expressed in the intestine and is likely secret
15 NRFs thereby coordinate the expression of nuclear and mi
16 interact with nuclear respiratory factor 1 (NRF-1) and activate NRF-1 target genes required for resp
21 ription factor nuclear respiratory factor 1 (NRF-1) to the cytochrome c promoter and NRF-2 to the cyt
23 iption factor, nuclear respiratory factor 1 (NRF-1), found recently by our laboratory to regulate all
29 (E(2)) induces nuclear respiratory factor-1 (NRF-1) transcription through ERalpha in MCF-7 breast can
30 these genes - nuclear respiratory factor-1 (NRF-1) was significantly up-regulated during the 4-OH-E2
31 on of multiple nuclear respiratory factor-1 (NRF-1)-dependent genes encoding key enzymes in oxidative
36 nduces increased expression of PGC-1, NRF-1, NRF-2, and mtTFA, factors that have been implicated in m
37 Inr), several known motifs (YY1, Sp1, NRF-1, NRF-2, CAAT, and CREB) and one potentially new motif (mo
38 equence-specific activators including NRF-1, NRF-2, Sp1, YY1, CREB and MEF-2/E-box factors, among oth
39 sted the hypothesis that increases in PGC-1, NRF-1, and NRF-2 are involved in the initial adaptive re
40 se findings suggest that increases in PGC-1, NRF-1, and NRF-2 represent key regulatory components of
41 tubes induces increased expression of PGC-1, NRF-1, NRF-2, and mtTFA, factors that have been implicat
42 activity, mRNA expression of the PGC-1alpha, NRF-1, Tfam and CytC genes, mitochondrial DNA content, m
44 vels for nuclear respiratory factor 1 and 2 (NRF-1 and -2), the proteins that are known to interact w
52 ar respiratory factor 1 (NRF-1) and activate NRF-1 target genes required for respiratory chain expres
54 eased nuclear respiratory factor activation (NRF-1 and NRF-2) and Tfam, TFB1M, and TFB2M mRNA express
57 , which is consistent with the absence of an NRF-1 consensus sequence in the proximal rat promoter.
58 litated expression via a "cargo" of AP-1 and NRF-1 transcription factors and TALE-based transcription
60 mitochondrial biogenesis and that NRF-1 and NRF-2 act as transcriptional activators of genes encodin
61 ection of genes controlled by both NRF-1 and NRF-2 and disfavor its membership in the immediate early
63 ercise induced increases in muscle NRF-1 and NRF-2 that were evident 12 to 18 h after one exercise bo
65 ed by nuclear respiratory factors (NRF-1 and NRF-2), key transcription factors implicated in mitochon
67 pothesis that increases in PGC-1, NRF-1, and NRF-2 are involved in the initial adaptive response of m
68 suggest that increases in PGC-1, NRF-1, and NRF-2 represent key regulatory components of the stimula
70 ed staining intensity with rhodamine 123 and NRF-1(-/-) blastocysts had markedly reduced levels of mi
71 lear-encoded metabolic genes, PGC-1alpha and NRF-1, was also observed in Stat3-null keratinocytes; ho
75 ich binds to DNA through its Ets domain, and NRF-2beta, which contains the transcription activation d
81 r 1 (NRF-1) to the cytochrome c promoter and NRF-2 to the cytochrome oxidase subunit 4 promoter incre
82 osphorylated RNA polymerase II, YY1, Sp1 and NRF-1, further suggesting a key role for NRF-1 in regula
85 tion of cellular NRF by expressing antisense NRF increased basal iNOS promoter activity and resulted
86 f ERbeta revealed that ERbeta inhibits basal NRF-1 expression and is required for 4-OHT-induced NRF-1
89 o the collection of genes controlled by both NRF-1 and NRF-2 and disfavor its membership in the immed
98 coded mitochondrial transcription factors by NRFs and PGC-1 family coactivators is essential to the c
99 off expression system, reduction of cellular NRF by expressing antisense NRF increased basal iNOS pro
104 Thus, NRF-1 and our previously described NRF-2 prove to be the two key bigenomic coordinators for
107 of motifs, including GABPA, MYC, E2F1, E2F4, NRF-1, CCAAT, YY1, and ACTACAnnTCC are overrepresented i
108 with high developmental expression of either NRF-1 (brown fat and developing brain) or myogenin (stri
109 with transcription factors such as ERRalpha, NRF-1, and HNF4alpha, however acetylation and transcript
111 data from 29 tissues indicate that the ETS, NRF-1, and Clus1 sequences that cluster are predominantl
112 rate that methylation of the CpG in the ETS, NRF-1, and SP1 motifs prevent DNA binding in nuclear ext
113 nscriptional activity suggests that the EWG, NRF-1, and P3A2 family of proteins shares common mechani
114 clear factor-erythroid 2 p45-related factor (NRF) 2 in the nucleus, which was associated with increas
117 y, we found that nuclear respiratory factor (NRF)-1, a key transcription factor for mitochondrial bio
119 moter identified nuclear respiratory factor (NRF)-1/alpha-PAL as a major player in regulating VSNL1 m
120 included Nfe2l2, nuclear respiratory factor (NRF)-2 (Gabpa), and MEF2, and for IL1Ra, included NRF-1
124 mediated by binding of transcription factors NRF-1 and CCAAT/enhancer-binding protein delta (C/EBP) t
126 is governed by nuclear respiratory factors (NRF-1 and NRF-2), key transcription factors implicated i
127 wders (MPP) were added to normal rice flour (NRF) and glutinous rice flour (GRF) at three levels (400
131 e consistent with a specific requirement for NRF-1 in the maintenance of mtDNA and respiratory chain
133 reover, genetic evidence supports a role for NRF-1 in the maintenance of mtDNA during embryonic devel
134 These findings disclose a novel role for NRF-1 in the transcriptional control of Complex II and p
138 nts confirmed the presence of two functional NRF-2 sites arranged in a tandem repeat, as well as a NR
140 , PGC-1alpha and the PGC-1alpha target gene, NRF-1 by binding to insulin response sequences in the PG
142 ilencing, and chromatin immunoprecipitation, NRF-1 was found to bind to the gene promoters of two of
145 se results show that an isolated increase in NRF-1 is not sufficient to bring about a coordinated inc
149 veral sequence-specific activators including NRF-1, NRF-2, Sp1, YY1, CREB and MEF-2/E-box factors, am
150 with multiple regulatory proteins, including NRF-1, which regulates genes involved in mitochondrial a
152 4-OHT), with an EC(50) of ~1.7 nM, increases NRF-1 expression by recruiting ERbeta, cJun, cFos, CBP,
157 esis in rat liver, we found that LPS induces NRF-1 protein expression and activity accompanied by mRN
159 omoter regions of COX6A(H) and COX7A(H) lack NRF sites but have conserved myocyte enhancer factor 2 (
161 d nuclear factor (erythroid-derived 2)-like (NRF)-2 (UPR-induced antioxidant protein) and increased c
162 higher hepatic TNF-alpha mRNA levels, lower NRF-1 and PGC-1alpha mRNA levels, and no enhancement of
165 The exercise induced increases in muscle NRF-1 and NRF-2 that were evident 12 to 18 h after one e
167 stress was also induced by dominant negative NRF-1 and by glucose deprivation, suggesting that divers
168 site and transfection of a dominant-negative NRF-1 both revealed the crucial role of NRF-1 in activat
169 as further confirmed using dominant-negative NRF-1 overexpression and NRF-1 small interfering RNA kno
170 -1 target genes by using a dominant-negative NRF-1 prevented c-Myc-induced apoptosis, without affecti
178 ty supershift assays demonstrated binding of NRF-2 to the other four subunits, and promoter mutation
180 PPARGC1 and PGC1-beta/PERC), coactivators of NRF-1 and PPAR gamma-dependent transcription, is decreas
181 nsfection of dominant-negative constructs of NRF-2 proteins caused a significant reduction of COX exp
182 can also PARylate the DNA-binding domain of NRF-1 and negatively regulate NRF-1.PARP-1 interaction.
183 show that DNA-binding/dimerization domain of NRF-1 and the N-terminal half of PARP-1, which contains
185 y be responsible for decreased expression of NRF-dependent genes, leading to the metabolic disturbanc
189 binding sequence (T/C)GCGCA(C/T)GCGC(A/G) of NRF-1 includes a noncanonical CA(C/T)GCG Myc:MAX binding
190 -2beta form a complex, the nuclear import of NRF-2alphabeta becomes strictly dependent on the NLS wit
191 we establish a link between the induction of NRF-1 target genes and sensitization to apoptosis on ser
192 lective interference with c-Myc induction of NRF-1 target genes by using a dominant-negative NRF-1 pr
193 OHT-induced apoptosis and siRNA knockdown of NRF-1 increased apoptosis, indicating an antiapoptotic r
194 te in the hiNOS promoter resulted in loss of NRF binding and increased basal but not cytokine-stimula
197 ivo genomic footprinting showed occupancy of NRF-2 and Sp1 consensus sites on the promoter of rat Tfa
202 b1 induced by KCl, whereas overexpression of NRF-1 rescued these transcripts from being suppressed by
203 nd COX induced by KCl, and overexpression of NRF-1 rescued these transcripts that were suppressed by
207 te oxidation-reduction (redox) regulation of NRF-1 in Tfam expression, blockade of upstream phosphati
208 is study discloses novel redox regulation of NRF-1 phosphorylation and nuclear translocation by phosp
209 e treated rats, as shown by up-regulation of NRF-2-dependent gene expression and down-regulation of p
212 t provides new insight regarding the role of NRF-1 was that expression of MEF2A and GLUT4 was increas
214 itively regulated by NRF-1, and silencing of NRF-1 with small interference RNA blocked the up-regulat
219 NRF-1 resulted in increased transcription of NRF-1 target CAPNS1 but not CYC1, CYC2, or TFAM despite
220 has been associated with the integration of NRFs and other transcription factors in a program of mit
221 g positive correlation between PGC-1alpha or NRF-1 and long IDE isoform transcripts was found in non-
223 ria-rich rat hepatoma cells that overexpress NRF-1, basal and oxidant-induced increases were found in
227 r mutations, and real-time quantitative PCR, NRF-1 was found to functionally bind to the promoters of
228 al analysis, and real-time quantitative PCR, NRF-1 was found to functionally bind to the promoters of
230 osed of two distinct and unrelated proteins: NRF-2alpha, which binds to DNA through its Ets domain, a
232 rent study, we identified in silico putative NRF-2 binding sites on all ten nuclear-encoded COX gene
234 sistent with a pathway whereby PRC regulates NRF-2-dependent genes through a multiprotein complex inv
235 tor 2 (NRF2; also called NFE2L2) and related NRF family members regulate antioxidant defenses by acti
237 matin immunoprecipitation assays also showed NRF-1 binding to all ten promoters in murine neuroblasto
241 TA and Inr), several known motifs (YY1, Sp1, NRF-1, NRF-2, CAAT, and CREB) and one potentially new mo
242 1 promotes mitochondrial biogenesis and that NRF-1 and NRF-2 act as transcriptional activators of gen
246 osphorylation, we tested the hypothesis that NRF-1 regulates Complex II expression and opposes hypoxi
248 ings are consistent with our hypothesis that NRF-2, in addition to regulating the coupling between ne
252 They also provide the new information that NRF-1 overexpression results in increased expression of
253 e model that explains these findings is that NRF-5 binds fluoxetine and influences its presentation o
256 omatin immunoprecipitation assay showed that NRF-2 bound in vivo to six of the ten nuclear-encoded CO
258 form a complex with PARP-1, suggesting that NRF-1 can recruit the PARP-1.DNA-PK.Ku80.Ku70.topoisomer
273 3.5-day-old embryos, demonstrating that the NRF-1 gene is expressed during oogenesis and during earl
275 ffordable foods and food groups by using the NRF index and US Department of Agriculture (USDA) nutrie
277 lastocysts can develop further in vitro, the NRF-1(-/-) blastocysts lack this ability despite their n
279 ter did not form a specific complex with the NRF-1 in the liver or hepatoma nuclear extracts, which i
283 onal relative of PGC-1 that operates through NRF-1 and possibly other activators in response to proli
288 These data demonstrate that the transacting NRF protein is involved in constitutive silencing of the
289 ive stress stimulates biogenesis in part via NRF-1 activation and corresponding to recovery events af
291 ocalization; however, the mechanism by which NRF-2 is imported into the nucleus remains unknown.
293 HCF-1 in vivo, and all three associate with NRF-2-dependent nuclear genes that direct the expression
297 d in all ATL cases physically interacts with NRF-1 and inhibits the DNA-binding ability of NRF-1.
298 zation signals (NLSs): the Ets domain within NRF-2alpha and the NLS within NRF-2beta (amino acids 311
299 domain within NRF-2alpha and the NLS within NRF-2beta (amino acids 311/321: EEPPAKRQCIE) that is rec
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