ライフサイエンスコーパス: NRF

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

17 ns a conserved nuclear respiratory factor 1 (NRF-1) binding site.

18 Nuclear respiratory factor 1 (NRF-1) is a transcriptional activator of nuclear genes t

19 Nuclear respiratory factor 1 (NRF-1) is one of the key transcriptional activators for

20 ypothesis that nuclear respiratory factor 1 (NRF-1) serves such a role in subunit coordination.

21 ription factor nuclear respiratory factor 1 (NRF-1) to the cytochrome c promoter and NRF-2 to the cyt

22 tive allele of nuclear respiratory factor 1 (NRF-1), and glucose deprivation.

23 iption factor, nuclear respiratory factor 1 (NRF-1), found recently by our laboratory to regulate all

24 Nuclear respiratory factor 1 (NRF-1), which induces nuclear-encoded mitochondrial gene

25 iption factor, nuclear respiratory factor 1 (NRF-1), which regulates all COX subunit genes.

26 teraction with nuclear respiratory factor 1 (NRF-1).

27 species, i.e. nuclear respiratory factor-1 (NRF-1) and mitochondrial transcription factor-A.

28 Nuclear respiratory factor-1 (NRF-1) is integral to the transcriptional regulation of

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

32 fic binding to nuclear respiratory factor-1 (NRF-1).

33 1 (PGC-1), and nuclear respiratory factor-1 (NRF-1).

34 ription factor nuclear respiratory factor-1 (NRF-1).

35 Notably, recognition sites for NRF-1, NRF-2 and Sp1 are common to most nuclear genes encoding

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

43 mitochondrial biogenesis pathway (PGC-1alpha/NRF-1).

44 vels for nuclear respiratory factor 1 and 2 (NRF-1 and -2), the proteins that are known to interact w

45 Nuclear respiratory factor 2 (NRF-2) is a mammalian transcription factor composed of t

46 ding sites for nuclear respiratory factor 2 (NRF-2) on the promoter of exon IX.

47 ctors, such as nuclear respiratory factor 2 (NRF-2).

48 n mitochondrial biogenesis (PGC-1alpha, 55%; NRF-1, 15%; TFAM, 85%).

49 nsthyretin protein TTR-52, as well as CED-7, NRF-5 and CED-6.

50 es arranged in a tandem repeat, as well as a NRF-1 site and an Sp1 site.

51 at which site-directed mutagenesis abolished NRF-1 phosphorylation by Akt.

52 ar respiratory factor 1 (NRF-1) and activate NRF-1 target genes required for respiratory chain expres

53 shown to interact with NRF-1 and co-activate NRF-1.

54 eased nuclear respiratory factor activation (NRF-1 and NRF-2) and Tfam, TFB1M, and TFB2M mRNA express

55 tor-erythroid-derived 2-like 2 (NFE2L2 alias NRF-2).

56 Although NRF-1 expression is decreased only in diabetic subjects,

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

59 NRF-1 and NRF-2 act additively while NRF-2 synergizes with CREB/AT

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

62 nd mtTFA protein expression and in NRF-1 and NRF-2 binding to DNA.

63 ercise induced increases in muscle NRF-1 and NRF-2 that were evident 12 to 18 h after one exercise bo

64 ear respiratory factor activation (NRF-1 and NRF-2) and Tfam, TFB1M, and TFB2M mRNA expression.

65 ed by nuclear respiratory factors (NRF-1 and NRF-2), key transcription factors implicated in mitochon

66 We conclude that Sp1, NRF-1, and NRF-2 are important in activating transcription of the r

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

69 or the transcription factors Sp1, NRF-1, and NRF-2.

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

72 We show that both NRF-2alpha and NRF-2beta contain intrinsic nuclear localization signals

73 When NRF-2alpha and NRF-2beta form a complex, the nuclear import of NRF-2alp

74 Both CREB and NRF-1 bind the same sites on PRC, and the interaction wi

75 ich binds to DNA through its Ets domain, and NRF-2beta, which contains the transcription activation d

76 g dominant-negative NRF-1 overexpression and NRF-1 small interfering RNA knockdown.

77 Finally, Akt phosphorylation and NRF-1 translocation predictably lacked oxidant regulatio

78 nt, mediates the association between PRC and NRF-2.

79 Both PRC and NRF-2beta bind HCF-1 in vitro, and the molecular determi

80 In addition, PRC and NRF-2beta can complex with HCF-1 in vivo, and all three

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

83 While most isolated wild-type and NRF-1(+/-) blastocysts can develop further in vitro, the

84 rs (TFs) SP1, NF-Y, ETS, CREB, TBP, USF, and NRF-1.

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

87 Surprisingly, neither coactivator binds NRF-2(GABP), a multisubunit transcriptional activator as

88 s through cis-acting elements that bind both NRF-1 and CREB.

89 o the collection of genes controlled by both NRF-1 and NRF-2 and disfavor its membership in the immed

90 asing in retrogradation was observed in both NRF and GRF with MPP added of all levels.

91 We show that both NRF-2alpha and NRF-2beta contain intrinsic nuclear local

92 DNA-bound NRF-1 can form a complex with PARP-1, suggesting that NR

93 PRC trans-activation through promoter-bound NRF-2.

94 a role during transcriptional activation by NRF-1.

95 Atp1b1 is positively regulated by NRF-1, and silencing of NRF-1 with small interference RN

96 ther hand, Atp1a1 is negatively regulated by NRF-1.

97 aspect of transcriptional regulation used by NRF-1.

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

100 In A549 and HeLa human cells, constitutive NRF mRNA expression is detected by RT-PCR.

101 Gel shift assay showed constitutive NRF binding to the hiNOS NRE.

102 genes to transcription factories containing NRF's and YY1.

103 Moreover, a CREB/NRF-1 interaction domain on PRC is required for its tran

104 Thus, NRF-1 and our previously described NRF-2 prove to be the two key bigenomic coordinators for

105 noprecipitation provided evidence for direct NRF-1 binding to the VSNL1 promoter.

106 ssion of Bdnf exon IX, whereas knocking down NRF-2 down-regulated such expression.

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

110 iants of six known CpG-containing TFBS: ETS, NRF-1, BoxA, SP1, CRE, and E-Box.

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

115 NF-kappaB-repressing factor (NRF) interacts with a specific negative regulatory eleme

116 or the cellular NF-kappaB-repressing factor (NRF).

117 y, we found that nuclear respiratory factor (NRF)-1, a key transcription factor for mitochondrial bio

118 and protein for nuclear respiratory factor (NRF)-1.

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

121 ding activity of nuclear respiratory factor (NRF)-2.

122 osphorylation of nuclear respiratory factor (NRF-1) and binding to the Tfam promoter.

123 RC1 and PCNA, and the transcription factor - NRF-1.

124 mediated by binding of transcription factors NRF-1 and CCAAT/enhancer-binding protein delta (C/EBP) t

125 sites detected nuclear respiratory factors (NRF's) and YY1 specifically on the paternal allele.

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

128 the development of the Nutrient-Rich Foods (NRF) family of nutrient profile models.

129 The Nutrient Rich Foods (NRF) Index is a formal scoring system that ranks foods o

130 Embryos homozygous for NRF-1 disruption die between embryonic days 3.5 and 6.5.

131 e consistent with a specific requirement for NRF-1 in the maintenance of mtDNA and respiratory chain

132 and NRF-1, further suggesting a key role for NRF-1 in regulation of the SNRPN locus.

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

135 ptosis, indicating an antiapoptotic role for NRF-1.

136 We have also elucidated a role for NRF-2 as a regulator of FMR1 in vivo through a previousl

137 Notably, recognition sites for NRF-1, NRF-2 and Sp1 are common to most nuclear genes en

138 nts confirmed the presence of two functional NRF-2 sites arranged in a tandem repeat, as well as a NR

139 nscription factor-A, mtDNA polymerase gamma, NRF-2, and single-stranded DNA-binding protein.

140 , PGC-1alpha and the PGC-1alpha target gene, NRF-1 by binding to insulin response sequences in the PG

141 The HBZ/NRF-1/TDP1 axis provides new therapeutic targets against

142 ilencing, and chromatin immunoprecipitation, NRF-1 was found to bind to the gene promoters of two of

143 synthase was increased approximately 50% in NRF-1 transgenic muscle.

144 in PGC-1 and mtTFA protein expression and in NRF-1 and NRF-2 binding to DNA.

145 se results show that an isolated increase in NRF-1 is not sufficient to bring about a coordinated inc

146 The 4-OHT-induced increase in NRF-1 resulted in increased transcription of NRF-1 targe

147 pression of MEF2A and GLUT4 was increased in NRF-1 transgenic muscle.

148 2 (Gabpa), and MEF2, and for IL1Ra, included NRF-1 and MEF2.

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

151 ut not CYC1, CYC2, or TFAM despite increased NRF-1 coactivator PGC-1alpha protein.

152 4-OHT), with an EC(50) of ~1.7 nM, increases NRF-1 expression by recruiting ERbeta, cJun, cFos, CBP,

153 bility shift and supershift assays indicated NRF-1 binding to all ten promoters.

154 An AP-1 inhibitor blocked 4-OHT-induced NRF-1 expression.

155 expression and is required for 4-OHT-induced NRF-1 transcription.

156 -1 site contributes to maximal 4-OHT-induced NRF-1 transcription.

157 esis in rat liver, we found that LPS induces NRF-1 protein expression and activity accompanied by mRN

158 HBZ suppresses TDP1 expression by inhibiting NRF-1 function in ATL cells.

159 omoter regions of COX6A(H) and COX7A(H) lack NRF sites but have conserved myocyte enhancer factor 2 (

160 Here, we demonstrate that, like NRF-1, CREB binds PRC in vitro and exists in a complex w

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

163 Moreover, NRF-1 is known to activate mitochondrial transcription f

164 Moreover, NRF-1 was immunoprecipitated from cell extracts by antib

165 The exercise induced increases in muscle NRF-1 and NRF-2 that were evident 12 to 18 h after one e

166 Like c-Myc, NRF-1 overexpression sensitizes cells to apoptosis on se

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

171 hereas the introduction of dominant-negative NRF-1 repressed such activity.

172 The ensuing accumulation of nuclear NRF-1 protein leads to gene activation for mitochondrial

173 RF-1 and inhibits the DNA-binding ability of NRF-1.

174 Activation of NRF-1 in fibroblasts has been shown to induce increases

175 eraction with NRF-1 and in the activation of NRF-1 target genes.

176 The activity of NRF-2 in neurons is regulated by nuclear localization; h

177 Specific binding of NRF-1 to Tfam promoter was demonstrated by electrophoret

178 ty supershift assays demonstrated binding of NRF-2 to the other four subunits, and promoter mutation

179 In vivo binding of NRF-2 to the rCOX6A1 promoter was confirmed with chromat

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

184 Moreover, the embryonic expression of NRF-1 did not result from maternal carryover.

185 y be responsible for decreased expression of NRF-dependent genes, leading to the metabolic disturbanc

186 We investigated here the in vivo function of NRF-1 in mammals by disrupting the gene in mice.

187 The function of NRF-1 was further confirmed using dominant-negative NRF-

188 binding sites confirmed the functionality of NRF-1 binding on all ten COX promoters.

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

195 nished oxidant production and caused loss of NRF-1 expression and growth delay.

196 Therefore, the nuclear import mechanism of NRF-2 is unique among Ets factors.

197 ivo genomic footprinting showed occupancy of NRF-2 and Sp1 consensus sites on the promoter of rat Tfa

198 Interestingly, overexpression of NRF suppressed both basal and cytokine-induced hiNOS pro

199 Overexpression of NRF-1 also upregulated endogenous TDP-1 expression, whil

200 Overexpression of NRF-1 increased TDP1-promoter activity, whereas the intr

201 Overexpression of NRF-1 inhibited 4-OHT-induced apoptosis and siRNA knockd

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

204 e, we dissect the nuclear import pathways of NRF-2.

205 o a lack of Akt-dependent phosphorylation of NRF-1 with 4-OHT treatment.

206 The presence of NRF's also suggests a link between transcriptional regul

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

210 tive NRF-1 both revealed the crucial role of NRF-1 in activation of P1.

211 To further evaluate the role of NRF-1 in the regulation of mitochondrial biogenesis and

212 t provides new insight regarding the role of NRF-1 was that expression of MEF2A and GLUT4 was increas

213 Silencing of NRF-1 with RNA interference reduced all ten COX subunit

214 itively regulated by NRF-1, and silencing of NRF-1 with small interference RNA blocked the up-regulat

215 However, silencing of NRF-1 with small interference RNA blocked the upregulati

216 The binding sites of NRF-1 on Atp1a1 and Atp1b1 are conserved among mice, rat

217 The binding sites of NRF-2 are conserved between rats and mice.

218 o demonstrate loss of oxidant stimulation of NRF-1 phosphorylation and Tfam expression.

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-

222 Overall, NRF-1 expression and activity is regulated by 4-OHT via

223 ria-rich rat hepatoma cells that overexpress NRF-1, basal and oxidant-induced increases were found in

224 ted from rat hepatoma cells that overexpress NRF-1.

225 Overexpressing NRF-2 up-regulated the expression of Bdnf exon IX, where

226 we generated transgenic mice overexpressing NRF-1 in skeletal muscle.

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

229 Cyclin D1-dependent kinase phosphorylates NRF-1 at S47.

230 osed of two distinct and unrelated proteins: NRF-2alpha, which binds to DNA through its Ets domain, a

231 Site-directed mutagenesis of putative NRF-1 binding sites confirmed the functionality of NRF-1

232 rent study, we identified in silico putative NRF-2 binding sites on all ten nuclear-encoded COX gene

233 ding domain of NRF-1 and negatively regulate NRF-1.PARP-1 interaction.

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

236 Second, NRF model performance was repeatedly tested against the

237 matin immunoprecipitation assays also showed NRF-1 binding to all ten promoters in murine neuroblasto

238 SIGNIFICANCE: NRF-1 mediates the tight coupling of neuronal activity,

239 ing sites for the transcription factors Sp1, NRF-1, and NRF-2.

240 We conclude that Sp1, NRF-1, and NRF-2 are important in activating transcripti

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

243 We conclude that NRF-1 plays a significant role in coordinating the trans

244 We conclude that NRF-2 is an important mediator of coordinated regulation

245 We show here that NRF-1 can also directly interact with poly(ADP-ribose) p

246 osphorylation, we tested the hypothesis that NRF-1 regulates Complex II expression and opposes hypoxi

247 To test our hypothesis that NRF-2 also regulates the Bdnf gene, we performed electro

248 ings are consistent with our hypothesis that NRF-2, in addition to regulating the coupling between ne

249 These results indicate that NRF-1 is a positive transcriptional regulator of TDP1-ge

250 Results indicate that NRF-2 functionally regulates exon IX of the rat Bdnf gen

251 Our results further indicated that NRF-1 could be a regulatory factor for gene expression o

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

254 We postulated that NRF-1 suppression either specifically decreases the expr

255 In addition, we show that NRF recognition sites within both TFB promoters are requ

256 omatin immunoprecipitation assay showed that NRF-2 bound in vivo to six of the ten nuclear-encoded CO

257 These results suggest that NRF's and YY1 may facilitate PWS-IC function and coordin

258 form a complex with PARP-1, suggesting that NRF-1 can recruit the PARP-1.DNA-PK.Ku80.Ku70.topoisomer

259 The NRF-2beta NLS contains only two lysine/arginine residues

260 The NRF-5 protein is homologous to a family of secreted lipi

261 consensus HCF-1 binding site on PRC and the NRF-2 activation domain.

262 plex formed between the rat promoter and the NRF-2 protein was comparable in the two extracts.

263 First, the NRF models included nutrients to encourage as well as nu

264 However, the NRF-2 subunits and PRC are co-immunoprecipitated from ce

265 antioxidant response elements (AREs) in the NRF-1 promoter.

266 espiratory capacity was not increased in the NRF-1 transgenic mice.

267 Examination of the NRF-1 amino acid sequence revealed an Akt phosphorylatio

268 A portion of the NRF-1 gene that encodes the nuclear localization signal

269 idase expression is under the control of the NRF-1 promoter.

270 Methylation of the NRF-1-binding site was found to be able to regulate VSNL

271 Two of the NRF-2 sites in this basal promoter are organized in a ta

272 s is not required for the recognition of the NRF-2beta NLS.

273 3.5-day-old embryos, demonstrating that the NRF-1 gene is expressed during oogenesis and during earl

274 We conclude that the NRF-2beta NLS is an unusual but is, nevertheless, a bona

275 ffordable foods and food groups by using the NRF index and US Department of Agriculture (USDA) nutrie

276 Dietary Studies 1.0 were scored by using the NRF index.

277 lastocysts can develop further in vitro, the NRF-1(-/-) blastocysts lack this ability despite their n

278 PRC interacts in vitro with the NRF-1 DNA binding domain through two distinct recognitio

279 ter did not form a specific complex with the NRF-1 in the liver or hepatoma nuclear extracts, which i

280 Possible interactions between the NRFs will be investigated in the future.

281 n study confirmed the functionality of these NRF-2 binding sites.

282 This NRF algorithm was represented by the sum of the percenta

283 onal relative of PGC-1 that operates through NRF-1 and possibly other activators in response to proli

284 Thus, NRF-1 and our previously described NRF-2 prove to be the

285 Thus, NRF-1 is an essential transcription factor critical in t

286 Thus, NRF-1 regulates key Na(+)/K(+)-ATPase subunits and plays

287 Thus, NRF-1 was implicated in oxidant-mediated mitochondrial b

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

290 When NRF-2alpha and NRF-2beta form a complex, the nuclear imp

291 ocalization; however, the mechanism by which NRF-2 is imported into the nucleus remains unknown.

292 NRF-1 and NRF-2 act additively while NRF-2 synergizes with CREB/ATF at FMR1's promoter.

293 HCF-1 in vivo, and all three associate with NRF-2-dependent nuclear genes that direct the expression

294 have previously been shown to interact with NRF-1 and co-activate NRF-1.

295 to PGC-1, especially in its interaction with NRF-1 and in the activation of NRF-1 target genes.

296 is in part through a direct interaction with NRF-1.

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

300 becomes strictly dependent on the NLS within NRF-2beta.