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1                                              NRF-1 and NRF-2 act additively while NRF-2 synergizes wi
2                                              NRF-1 and Sp1 are known to bind and stimulate the active
3                                              NRF-1 binding sites on Grin1 and Grin2b genes are also h
4                                              NRF-1 expression and growth were restored by exogenous o
5                                              NRF-1 functionally regulates mediators of energy consump
6                                              NRF-1 gene silencing blocked aerobic succinate oxidation
7                                              NRF-1 gene silencing produced 1:1 knockdown of Tfam expr
8                                              NRF-1 regulates mediators of neuronal activity and energ
9                                              NRF-1 transcriptionally regulates Na(+)/K(+)-ATPase subu
10                                              NRF-1 was required for stable binding of Sp1.
11                                              NRF-1, cAMP response element, and Sp-1 site mutations wi
12                                              NRF-1-Tfam binding was augmented under pro-oxidant condi
13  interact with nuclear respiratory factor 1 (NRF-1) and activate NRF-1 target genes required for resp
14 owed that both nuclear respiratory factor 1 (NRF-1) and cAMP-response element-binding protein (CREB)
15 ncluding human nuclear respiratory factor 1 (NRF-1) and the sea urchin P3A2 protein.
16 ns a conserved nuclear respiratory factor 1 (NRF-1) binding site.
17 ave implicated nuclear respiratory factor 1 (NRF-1) in the transcriptional expression of nuclear gene
18                Nuclear respiratory factor 1 (NRF-1) is a nuclear transcription factor that has been i
19                Nuclear respiratory factor 1 (NRF-1) is a transcriptional activator of nuclear genes t
20                Nuclear respiratory factor 1 (NRF-1) is a transcriptional activator that acts on a div
21                Nuclear respiratory factor 1 (NRF-1) is one of the key transcriptional activators for
22 ypothesis that nuclear respiratory factor 1 (NRF-1) serves such a role in subunit coordination.
23 ription factor nuclear respiratory factor 1 (NRF-1) to the cytochrome c promoter and NRF-2 to the cyt
24 tive allele of nuclear respiratory factor 1 (NRF-1), and glucose deprivation.
25 iption factor, nuclear respiratory factor 1 (NRF-1), found recently by our laboratory to regulate all
26 ding sites for nuclear respiratory factor 1 (NRF-1), nuclear respiratory factor 2/GA binding protein
27                Nuclear respiratory factor 1 (NRF-1), which induces nuclear-encoded mitochondrial gene
28 iption factor, nuclear respiratory factor 1 (NRF-1), which regulates all COX subunit genes.
29 teraction with nuclear respiratory factor 1 (NRF-1).
30 , c-jun, JunB, nuclear respiratory factor 1 (NRF-1)], mitochondrial proliferation [cytochrome c (Cyt
31  species, i.e. nuclear respiratory factor-1 (NRF-1) and mitochondrial transcription factor-A.
32 tional Sp1 and nuclear respiratory factor-1 (NRF-1) elements within a GC-rich proximal GluR2 promoter
33                Nuclear respiratory factor-1 (NRF-1) is integral to the transcriptional regulation of
34  a TATA box, a nuclear respiratory factor-1 (NRF-1) site, and two GC boxes.
35 s bound by the nuclear respiratory factor-1 (NRF-1) transcription factor.
36 (E(2)) induces nuclear respiratory factor-1 (NRF-1) transcription through ERalpha in MCF-7 breast can
37  these genes - nuclear respiratory factor-1 (NRF-1) was significantly up-regulated during the 4-OH-E2
38 on of multiple nuclear respiratory factor-1 (NRF-1)-dependent genes encoding key enzymes in oxidative
39 fic binding to nuclear respiratory factor-1 (NRF-1).
40 1 (PGC-1), and nuclear respiratory factor-1 (NRF-1).
41 ription factor nuclear respiratory factor-1 (NRF-1).
42 nB, as well as nuclear respiratory factor-1 (NRF-1).
43 sted the hypothesis that increases in PGC-1, NRF-1, and NRF-2 are involved in the initial adaptive re
44 se findings suggest that increases in PGC-1, NRF-1, and NRF-2 represent key regulatory components of
45 tubes induces increased expression of PGC-1, NRF-1, NRF-2, and mtTFA, factors that have been implicat
46 activity, mRNA expression of the PGC-1alpha, NRF-1, Tfam and CytC genes, mitochondrial DNA content, m
47 mitochondrial biogenesis pathway (PGC-1alpha/NRF-1).
48 vels for nuclear respiratory factor 1 and 2 (NRF-1 and -2), the proteins that are known to interact w
49         Nuclear respiratory factors 1 and 2 (NRF-1 and NRF-2) are ubiquitous transcription factors th
50 n mitochondrial biogenesis (PGC-1alpha, 55%; NRF-1, 15%; TFAM, 85%).
51 es arranged in a tandem repeat, as well as a NRF-1 site and an Sp1 site.
52          Mutagenesis studies revealed that a NRF-1 site is especially important for the basal and ind
53 at which site-directed mutagenesis abolished NRF-1 phosphorylation by Akt.
54 ar respiratory factor 1 (NRF-1) and activate NRF-1 target genes required for respiratory chain expres
55 shown to interact with NRF-1 and co-activate NRF-1.
56                                PRC activated NRF-1-dependent promoters in a manner similar to that ob
57 eased nuclear respiratory factor activation (NRF-1 and NRF-2) and Tfam, TFB1M, and TFB2M mRNA express
58                                     Although NRF-1 can dimerize in the absence of DNA, phosphorylatio
59                                     Although NRF-1 expression is decreased only in diabetic subjects,
60 n was accounted for by point mutations in an NRF-1 site and either of two flanking sites for Sp1.
61 , which is consistent with the absence of an NRF-1 consensus sequence in the proximal rat promoter.
62 litated expression via a "cargo" of AP-1 and NRF-1 transcription factors and TALE-based transcription
63 ed staining intensity with rhodamine 123 and NRF-1(-/-) blastocysts had markedly reduced levels of mi
64 lear-encoded metabolic genes, PGC-1alpha and NRF-1, was also observed in Stat3-null keratinocytes; ho
65                                Both CREB and NRF-1 bind the same sites on PRC, and the interaction wi
66                           Moreover, CREB and NRF-1 were phosphorylated sequentially in response to se
67 g dominant-negative NRF-1 overexpression and NRF-1 small interfering RNA knockdown.
68             Finally, Akt phosphorylation and NRF-1 translocation predictably lacked oxidant regulatio
69 luR2 promoter activity required both Sp1 and NRF-1 cis elements and an interelement nucleotide bridge
70 osphorylated RNA polymerase II, YY1, Sp1 and NRF-1, further suggesting a key role for NRF-1 in regula
71            While most isolated wild-type and NRF-1(+/-) blastocysts can develop further in vitro, the
72 rs (TFs) SP1, NF-Y, ETS, CREB, TBP, USF, and NRF-1.
73 om HepG2 cell nuclear extract, identified as NRF-1 and Sp1, bound to the promoter at sites within the
74 d competition experiments with the authentic NRF-1 and NRF-2 DNA oligomers from previously characteri
75 f ERbeta revealed that ERbeta inhibits basal NRF-1 expression and is required for 4-OHT-induced NRF-1
76 s through cis-acting elements that bind both NRF-1 and CREB.
77 o the collection of genes controlled by both NRF-1 and NRF-2 and disfavor its membership in the immed
78               The activation domains of both NRF-1 and NRF-2 were extensively characterized by both d
79                                    DNA-bound NRF-1 can form a complex with PARP-1, suggesting that NR
80  a role during transcriptional activation by NRF-1.
81  regulation of a signal transduction gene by NRF-1.
82 5 is the first gene shown to be regulated by NRF-1 that possesses an expression profile during embryo
83            Atp1b1 is positively regulated by NRF-1, and silencing of NRF-1 with small interference RN
84 ther hand, Atp1a1 is negatively regulated by NRF-1.
85 onal domains required for transactivation by NRF-1 have been defined.
86 aspect of transcriptional regulation used by NRF-1.
87                             Moreover, a CREB/NRF-1 interaction domain on PRC is required for its tran
88 noprecipitation provided evidence for direct NRF-1 binding to the VSNL1 promoter.
89 of motifs, including GABPA, MYC, E2F1, E2F4, NRF-1, CCAAT, YY1, and ACTACAnnTCC are overrepresented i
90 with high developmental expression of either NRF-1 (brown fat and developing brain) or myogenin (stri
91 with transcription factors such as ERRalpha, NRF-1, and HNF4alpha, however acetylation and transcript
92 iants of six known CpG-containing TFBS: ETS, NRF-1, BoxA, SP1, CRE, and E-Box.
93  data from 29 tissues indicate that the ETS, NRF-1, and Clus1 sequences that cluster are predominantl
94 rate that methylation of the CpG in the ETS, NRF-1, and SP1 motifs prevent DNA binding in nuclear ext
95 nscriptional activity suggests that the EWG, NRF-1, and P3A2 family of proteins shares common mechani
96 e data suggest that the transcription factor NRF-1 plays a key role in cellular adaptation to energy
97 osphorylation of nuclear respiratory factor (NRF-1) and binding to the Tfam promoter.
98 RC1 and PCNA, and the transcription factor - NRF-1.
99 al sites for the nuclear respiratory factors NRF-1 and NRF-2 were identified.
100 ns sites for the nuclear respiratory factors NRF-1 and NRF-2, which have been shown to contribute to
101 regulated by the nuclear respiratory factors NRF-1 and NRF-2.
102 mediated by binding of transcription factors NRF-1 and CCAAT/enhancer-binding protein delta (C/EBP) t
103  is governed by nuclear respiratory factors (NRF-1 and NRF-2), key transcription factors implicated i
104                       Embryos homozygous for NRF-1 disruption die between embryonic days 3.5 and 6.5.
105 spiration, but only if translatable mRNA for NRF-1 is available.
106 e consistent with a specific requirement for NRF-1 in the maintenance of mtDNA and respiratory chain
107  These results support a regulatory role for NRF-1 and possibly AP-1 in the initiation of mitochondri
108 and NRF-1, further suggesting a key role for NRF-1 in regulation of the SNRPN locus.
109 reover, genetic evidence supports a role for NRF-1 in the maintenance of mtDNA during embryonic devel
110     These findings disclose a novel role for NRF-1 in the transcriptional control of Complex II and p
111 ptosis, indicating an antiapoptotic role for NRF-1.
112               Notably, recognition sites for NRF-1, NRF-2 and Sp1 are common to most nuclear genes en
113 etic mobility shift assay using a functional NRF-1 binding site from the delta-aminolevulinate (ALA)
114 , PGC-1alpha and the PGC-1alpha target gene, NRF-1 by binding to insulin response sequences in the PG
115                                      The HBZ/NRF-1/TDP1 axis provides new therapeutic targets against
116 tially by c-jun (0.5-3 hr), JunB (0.5-6 hr), NRF-1 (1-12 hr), Cyt c (12-72 hr), and muscle-specific C
117 s to sequence heterogeneity within the human NRF-1 5'-untranslated region (UTR).
118 47kb, bringing the total length of the human NRF-1 gene to approx. 104kb.
119             These exons were mapped to human NRF-1 genomic clones and their sequences, including dono
120 ilencing, and chromatin immunoprecipitation, NRF-1 was found to bind to the gene promoters of two of
121                     A 10 out of 12 imperfect NRF-1 site was located within the first exon.
122  synthase was increased approximately 50% in NRF-1 transgenic muscle.
123 in PGC-1 and mtTFA protein expression and in NRF-1 and NRF-2 binding to DNA.
124 ent 5'-UTR exons (UTRs 1-6) were detected in NRF-1 transcripts.
125 se results show that an isolated increase in NRF-1 is not sufficient to bring about a coordinated inc
126 nsumption was associated with an increase in NRF-1 mRNA.
127   It was also associated with an increase in NRF-1 protein binding activity as determined by electrop
128                The 4-OHT-induced increase in NRF-1 resulted in increased transcription of NRF-1 targe
129 pression of MEF2A and GLUT4 was increased in NRF-1 transgenic muscle.
130 2 (Gabpa), and MEF2, and for IL1Ra, included NRF-1 and MEF2.
131 veral sequence-specific activators including NRF-1, NRF-2, Sp1, YY1, CREB and MEF-2/E-box factors, am
132 with multiple regulatory proteins, including NRF-1, which regulates genes involved in mitochondrial a
133 ut not CYC1, CYC2, or TFAM despite increased NRF-1 coactivator PGC-1alpha protein.
134 4-OHT), with an EC(50) of ~1.7 nM, increases NRF-1 expression by recruiting ERbeta, cJun, cFos, CBP,
135 bility shift and supershift assays indicated NRF-1 binding to all ten promoters.
136      An AP-1 inhibitor blocked 4-OHT-induced NRF-1 expression.
137 expression and is required for 4-OHT-induced NRF-1 transcription.
138 -1 site contributes to maximal 4-OHT-induced NRF-1 transcription.
139 esis in rat liver, we found that LPS induces NRF-1 protein expression and activity accompanied by mRN
140 HBZ suppresses TDP1 expression by inhibiting NRF-1 function in ATL cells.
141                Overexpression of full-length NRF-1 and a dominant-negative form of NRF-1 modulated re
142              Here, we demonstrate that, like NRF-1, CREB binds PRC in vitro and exists in a complex w
143  higher hepatic TNF-alpha mRNA levels, lower NRF-1 and PGC-1alpha mRNA levels, and no enhancement of
144         Mutations within human UTR1 modulate NRF-1 expression by interfering with mRNA translational
145                                    Moreover, NRF-1 is known to activate mitochondrial transcription f
146                                    Moreover, NRF-1 was immunoprecipitated from cell extracts by antib
147     The exercise induced increases in muscle NRF-1 and NRF-2 that were evident 12 to 18 h after one e
148                                  Like c-Myc, NRF-1 overexpression sensitizes cells to apoptosis on se
149 stress was also induced by dominant negative NRF-1 and by glucose deprivation, suggesting that divers
150 site and transfection of a dominant-negative NRF-1 both revealed the crucial role of NRF-1 in activat
151 as further confirmed using dominant-negative NRF-1 overexpression and NRF-1 small interfering RNA kno
152 -1 target genes by using a dominant-negative NRF-1 prevented c-Myc-induced apoptosis, without affecti
153 hereas the introduction of dominant-negative NRF-1 repressed such activity.
154          The ensuing accumulation of nuclear NRF-1 protein leads to gene activation for mitochondrial
155 RF-1 and inhibits the DNA-binding ability of NRF-1.
156                                Activation of NRF-1 in fibroblasts has been shown to induce increases
157 eraction with NRF-1 and in the activation of NRF-1 target genes.
158 finding is consistent with the appearance of NRF-1 and fos/jun mRNAs prior to that of Cyt c and sugge
159                      Physical association of NRF-1 protein with the NRF-1 enhancer element and of c-J
160                          Specific binding of NRF-1 to Tfam promoter was demonstrated by electrophoret
161 PPARGC1 and PGC1-beta/PERC), coactivators of NRF-1 and PPAR gamma-dependent transcription, is decreas
162  can also PARylate the DNA-binding domain of NRF-1 and negatively regulate NRF-1.PARP-1 interaction.
163 show that DNA-binding/dimerization domain of NRF-1 and the N-terminal half of PARP-1, which contains
164        Moreover, the embryonic expression of NRF-1 did not result from maternal carryover.
165 length NRF-1 and a dominant-negative form of NRF-1 modulated reporter gene expression driven by the c
166 We investigated here the in vivo function of NRF-1 in mammals by disrupting the gene in mice.
167  coactivates the transcriptional function of NRF-1 on the promoter for mitochondrial transcription fa
168                              The function of NRF-1 was further confirmed using dominant-negative NRF-
169 binding sites confirmed the functionality of NRF-1 binding on all ten COX promoters.
170 binding sequence (T/C)GCGCA(C/T)GCGC(A/G) of NRF-1 includes a noncanonical CA(C/T)GCG Myc:MAX binding
171 is the first demonstration that induction of NRF-1 and c-Jun by pacing of cardiac myocytes directly m
172     PGC-1 stimulates a powerful induction of NRF-1 and NRF-2 gene expression; in addition, PGC-1 bind
173 we establish a link between the induction of NRF-1 target genes and sensitization to apoptosis on ser
174 lective interference with c-Myc induction of NRF-1 target genes by using a dominant-negative NRF-1 pr
175 OHT-induced apoptosis and siRNA knockdown of NRF-1 increased apoptosis, indicating an antiapoptotic r
176 nished oxidant production and caused loss of NRF-1 expression and growth delay.
177                            Overexpression of NRF-1 also upregulated endogenous TDP-1 expression, whil
178                            Overexpression of NRF-1 increased TDP1-promoter activity, whereas the intr
179                            Overexpression of NRF-1 inhibited 4-OHT-induced apoptosis and siRNA knockd
180 b1 induced by KCl, whereas overexpression of NRF-1 rescued these transcripts from being suppressed by
181 nd COX induced by KCl, and overexpression of NRF-1 rescued these transcripts that were suppressed by
182 o a lack of Akt-dependent phosphorylation of NRF-1 with 4-OHT treatment.
183 te oxidation-reduction (redox) regulation of NRF-1 in Tfam expression, blockade of upstream phosphati
184 is study discloses novel redox regulation of NRF-1 phosphorylation and nuclear translocation by phosp
185 tive NRF-1 both revealed the crucial role of NRF-1 in activation of P1.
186              To further evaluate the role of NRF-1 in the regulation of mitochondrial biogenesis and
187 t provides new insight regarding the role of NRF-1 was that expression of MEF2A and GLUT4 was increas
188                                 Silencing of NRF-1 with RNA interference reduced all ten COX subunit
189 itively regulated by NRF-1, and silencing of NRF-1 with small interference RNA blocked the up-regulat
190                        However, silencing of NRF-1 with small interference RNA blocked the upregulati
191                         The binding sites of NRF-1 on Atp1a1 and Atp1b1 are conserved among mice, rat
192 o demonstrate loss of oxidant stimulation of NRF-1 phosphorylation and Tfam expression.
193 NRF-1 resulted in increased transcription of NRF-1 target CAPNS1 but not CYC1, CYC2, or TFAM despite
194 g positive correlation between PGC-1alpha or NRF-1 and long IDE isoform transcripts was found in non-
195                                     Overall, NRF-1 expression and activity is regulated by 4-OHT via
196 ria-rich rat hepatoma cells that overexpress NRF-1, basal and oxidant-induced increases were found in
197 ted from rat hepatoma cells that overexpress NRF-1.
198  we generated transgenic mice overexpressing NRF-1 in skeletal muscle.
199 al analysis, and real-time quantitative PCR, NRF-1 was found to functionally bind to the promoters of
200 r mutations, and real-time quantitative PCR, NRF-1 was found to functionally bind to the promoters of
201    Cyclin D1-dependent kinase phosphorylates NRF-1 at S47.
202        Site-directed mutagenesis of putative NRF-1 binding sites confirmed the functionality of NRF-1
203 ated in vitro by phosphorylating recombinant NRF-1 with purified casein kinase II.
204 ding domain of NRF-1 and negatively regulate NRF-1.PARP-1 interaction.
205 matin immunoprecipitation assays also showed NRF-1 binding to all ten promoters in murine neuroblasto
206                                SIGNIFICANCE: NRF-1 mediates the tight coupling of neuronal activity,
207 ing sites for the transcription factors Sp1, NRF-1, and NRF-2.
208                        We conclude that Sp1, NRF-1, and NRF-2 are important in activating transcripti
209 TA and Inr), several known motifs (YY1, Sp1, NRF-1, NRF-2, CAAT, and CREB) and one potentially new mo
210 1 promotes mitochondrial biogenesis and that NRF-1 and NRF-2 act as transcriptional activators of gen
211                             We conclude that NRF-1 plays a significant role in coordinating the trans
212                      Here, we establish that NRF-1 is a phosphoprotein in vivo.
213  genes, but there is no direct evidence that NRF-1 transduces a physiological signal into the product
214                            We show here that NRF-1 can also directly interact with poly(ADP-ribose) p
215 osphorylation, we tested the hypothesis that NRF-1 regulates Complex II expression and opposes hypoxi
216                   The findings indicate that NRF-1 and NRF-2 utilize similar hydrophobic structural m
217                  These results indicate that NRF-1 is a positive transcriptional regulator of TDP1-ge
218           Our results further indicated that NRF-1 could be a regulatory factor for gene expression o
219   They also provide the new information that NRF-1 overexpression results in increased expression of
220                           We postulated that NRF-1 suppression either specifically decreases the expr
221                              We propose that NRF-1, which has been shown by others to be expressed du
222  form a complex with PARP-1, suggesting that NRF-1 can recruit the PARP-1.DNA-PK.Ku80.Ku70.topoisomer
223 d sequentially in response to serum, and the NRF-1 phosphorylation was accompanied by an increase in
224 ence suggesting that interaction between the NRF-1 site and an upstream element contributes to expres
225                        We show that both the NRF-1 and NRF-2 binding sites are functional in COX7AL a
226                      Mutations in either the NRF-1 or in the two cyclic AMP response elements on the
227                             Mutations in the NRF-1 and CRE sites inhibited the induction by electrica
228 lation results in an intrinsic change in the NRF-1 dimer enhancing its ability to bind DNA.
229  antioxidant response elements (AREs) in the NRF-1 promoter.
230 espiratory capacity was not increased in the NRF-1 transgenic mice.
231 insertions of Alu-sq family members into the NRF-1 locus.
232                           Examination of the NRF-1 amino acid sequence revealed an Akt phosphorylatio
233                             A portion of the NRF-1 gene that encodes the nuclear localization signal
234 igonucleotide antisense to the region of the NRF-1 initiation codon; a scrambled oligonucleotide with
235 idase expression is under the control of the NRF-1 promoter.
236                           Methylation of the NRF-1-binding site was found to be able to regulate VSNL
237 l hydrophobic motifs within 40 residues, the NRF-1 domain spans about 40% of the molecule and appears
238  3.5-day-old embryos, demonstrating that the NRF-1 gene is expressed during oogenesis and during earl
239    Site-directed mutagenesis showed that the NRF-1 site is crucial for promoter activity providing th
240               Specific factor binding to the NRF-1 site and GC boxes were demonstrated by gel mobilit
241 lastocysts can develop further in vitro, the NRF-1(-/-) blastocysts lack this ability despite their n
242              PRC interacts in vitro with the NRF-1 DNA binding domain through two distinct recognitio
243 ysical association of NRF-1 protein with the NRF-1 enhancer element and of c-Jun with the cyclic AMP
244 ter did not form a specific complex with the NRF-1 in the liver or hepatoma nuclear extracts, which i
245 entify related coactivators that act through NRF-1, we searched the databases for sequences with simi
246 onal relative of PGC-1 that operates through NRF-1 and possibly other activators in response to proli
247                                        Thus, NRF-1 and our previously described NRF-2 prove to be the
248                                        Thus, NRF-1 is an essential transcription factor critical in t
249                                        Thus, NRF-1 regulates key Na(+)/K(+)-ATPase subunits and plays
250                                        Thus, NRF-1 was implicated in oxidant-mediated mitochondrial b
251 ere cloned from the screen were identical to NRF-1, a result that was confirmed by further electropho
252 ive stress stimulates biogenesis in part via NRF-1 activation and corresponding to recovery events af
253 that it is a third common factor, along with NRF-1 and NRF-2, to be associated with COX gene regulati
254  have previously been shown to interact with NRF-1 and co-activate NRF-1.
255 to PGC-1, especially in its interaction with NRF-1 and in the activation of NRF-1 target genes.
256 is in part through a direct interaction with NRF-1.
257 d in all ATL cases physically interacts with NRF-1 and inhibits the DNA-binding ability of NRF-1.
258          On the basis of its similarity with NRF-1 and IBR, nrf is likely involved in transcriptional

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