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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
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.

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