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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)
17 ave implicated nuclear respiratory factor 1 (NRF-1) in the transcriptional expression of nuclear gene
23 ription factor nuclear respiratory factor 1 (NRF-1) to the cytochrome c promoter and NRF-2 to the cyt
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
30 , c-jun, JunB, nuclear respiratory factor 1 (NRF-1)], mitochondrial proliferation [cytochrome c (Cyt
32 tional Sp1 and nuclear respiratory factor-1 (NRF-1) elements within a GC-rich proximal GluR2 promoter
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
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
48 vels for nuclear respiratory factor 1 and 2 (NRF-1 and -2), the proteins that are known to interact w
54 ar respiratory factor 1 (NRF-1) and activate NRF-1 target genes required for respiratory chain expres
57 eased nuclear respiratory factor activation (NRF-1 and NRF-2) and Tfam, TFB1M, and TFB2M mRNA express
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
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
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
77 o the collection of genes controlled by both NRF-1 and NRF-2 and disfavor its membership in the immed
82 5 is the first gene shown to be regulated by NRF-1 that possesses an expression profile during embryo
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
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
100 ns sites for the nuclear respiratory factors NRF-1 and NRF-2, which have been shown to contribute to
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
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
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
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
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
120 ilencing, and chromatin immunoprecipitation, NRF-1 was found to bind to the gene promoters of two of
125 se results show that an isolated increase in NRF-1 is not sufficient to bring about a coordinated inc
127 It was also associated with an increase in NRF-1 protein binding activity as determined by electrop
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
134 4-OHT), with an EC(50) of ~1.7 nM, increases NRF-1 expression by recruiting ERbeta, cJun, cFos, CBP,
139 esis in rat liver, we found that LPS induces NRF-1 protein expression and activity accompanied by mRN
143 higher hepatic TNF-alpha mRNA levels, lower NRF-1 and PGC-1alpha mRNA levels, and no enhancement of
147 The exercise induced increases in muscle NRF-1 and NRF-2 that were evident 12 to 18 h after one e
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
158 finding is consistent with the appearance of NRF-1 and fos/jun mRNAs prior to that of Cyt c and sugge
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
165 length NRF-1 and a dominant-negative form of NRF-1 modulated reporter gene expression driven by the c
167 coactivates the transcriptional function of NRF-1 on the promoter for mitochondrial transcription fa
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
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
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
187 t provides new insight regarding the role of NRF-1 was that expression of MEF2A and GLUT4 was increas
189 itively regulated by NRF-1, and silencing of NRF-1 with small interference RNA blocked the up-regulat
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-
196 ria-rich rat hepatoma cells that overexpress NRF-1, basal and oxidant-induced increases were found in
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
205 matin immunoprecipitation assays also showed NRF-1 binding to all ten promoters in murine neuroblasto
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
213 genes, but there is no direct evidence that NRF-1 transduces a physiological signal into the product
215 osphorylation, we tested the hypothesis that NRF-1 regulates Complex II expression and opposes hypoxi
219 They also provide the new information that NRF-1 overexpression results in increased expression of
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
234 igonucleotide antisense to the region of the NRF-1 initiation codon; a scrambled oligonucleotide with
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
241 lastocysts can develop further in vitro, the NRF-1(-/-) blastocysts lack this ability despite their n
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
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
257 d in all ATL cases physically interacts with NRF-1 and inhibits the DNA-binding ability of NRF-1.
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