ライフサイエンスコーパス: NRF-2

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

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

3 1-mediated nuclear export and degradation of Nrf 2.

4 delayed degradation compared with wild-type Nrf 2.

5 his interaction, resulting in the release of Nrf 2.

6 ls that control nuclear import and export of Nrf 2.

7 ith Crm1 and abrogation of nuclear export of Nrf 2.

8 leading to nuclear export and degradation of Nrf 2.

9 by the nuclear respiratory factors NRF-1 and NRF-2.

10 nt mice is not the result of compensation by Nrf-2.

11 injury site by increasing the expression of Nrf-2.

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

13 HO-1 expression is controlled by Nrf-2.

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

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

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

17 f nuclear factor-erythroid 2-related factor (Nrf-2), a master antioxidant transcription factor, and o

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

19 mitochondrial biogenesis and that NRF-1 and NRF-2 act as transcriptional activators of genes encodin

20 lity is that NF-E2-related factors, Nrf-1 or Nrf-2, activate globin gene expression in the absence of

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

22 t N-acetyl cysteine results in inhibition of Nrf-2 activation.

23 esults indicate that reoxygenation-dependent Nrf-2 activity facilitates ischemic preconditioning thro

24 and V, which contained lower levels of both NRF-2 alpha and CO activity; and 3) CO-rich puffs in lay

25 A partial NRF-2 alpha cDNA was isolated from a human brain cDNA li

26 In normal monkeys, patterns of NRF-2 alpha distribution resembled closely that of CO ac

27 with tetrodotoxin for 1 day to 2 weeks, both NRF-2 alpha expression and CO activity were reduced in d

28 on resembled closely that of CO activity: 1) NRF-2 alpha immunoreactivity was localized in both nucle

29 otoxin, there was a progressive reduction of NRF-2 alpha in deprived ocular dominance columns, in par

30 normal and visually deprived adult monkeys, NRF-2 alpha is regulated by neuronal activity at the tra

31 the present study examined the expression of NRF-2 alpha mRNA in normal and monocularly deprived adul

32 The expression pattern of NRF-2 alpha mRNA in the normal striate cortex paralleled

33 ere to determine whether the distribution of NRF-2 alpha subunit proteins correlated with that of CO

34 clonal antibodies specifically against human NRF-2 alpha subunit.

35 ayers II and III contained a higher level of NRF-2 alpha than CO-poor interpuffs.

36 gh CO activity, were labeled more densely by NRF-2 alpha than layers I, IVB, and V, which contained l

37 Riboprobes of NRF-2 alpha was generated and labeled with digoxigenin-1

38 tion of the alpha subunit proteins of NRF-2 (NRF-2 alpha) with CO in the monkey striate cortex, and t

39 ed by CO activity and that the expression of NRF-2 alpha, like that of CO, is regulated tightly by ne

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

41 T2DM versus non-T2DM OA cartilage (0.57-fold Nrf-2 and 0.34-fold HO-1), and prostaglandin E2 (PGE2) r

42 ection of genes controlled by both NRF-1 and NRF-2 and disfavor its membership in the immediate early

43 tered ATP levels, decreased glycolytic flux, Nrf-2 and glutathione levels, ultimately resulting in ca

44 Ex vivo experiments indicated that Nrf-2 and HO-1 expression is reduced in T2DM versus non-

45 expression of antioxidant enzymes, PI3K/Akt/Nrf-2 and intracellular ROS production were investigated

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

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

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

49 nduces increased expression of PGC-1, NRF-1, NRF-2, and mtTFA, factors that have been implicated in m

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

51 um, also induces ROS accumulation, activates Nrf-2, and upregulates Nrf-2 target gene expression in t

52 ver, COX-2 proinflammatory state, as well as Nrf-2 antioxidant impairment, triggers oxidative/nitrosa

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

54 icted to hematopoietic cells while Nrf-1 and Nrf-2 are expressed in a wide range of tissues.

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

56 pothesis that increases in PGC-1, NRF-1, and NRF-2 are involved in the initial adaptive response of m

57 clear respiratory factors 1 and 2 (NRF-1 and NRF-2) are ubiquitous transcription factors that have be

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

59 etion and mutation analysis suggested that a NRF-2 binding site at -94 to -101 and an E2F binding sit

60 We show that both the NRF-1 and NRF-2 binding sites are functional in COX7AL and present

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

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

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

64 ele resulted in increased YY-1 and decreased Nrf-2 binding to the p18 promoter as compared with the C

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

66 The results of these studies suggest that Nrf-2, bound to the PRE, plays an important regulatory r

67 Inr), several known motifs (YY1, Sp1, NRF-1, NRF-2, CAAT, and CREB) and one potentially new motif (mo

68 he Ets family, nuclear respiratory factor 2 (NRF-2), can activate in vitro the gene expression of cyt

69 Nrf 2 contains well defined signals that control nuclear

70 nuclear factor (erythroid derived-2) like2 (Nrf-2), cyclooxygenase 2 (COX-2) products, or lipoxin ac

71 Nrf-2-deficient mice had no detectable hematopoietic def

72 e treated rats, as shown by up-regulation of NRF-2-dependent gene expression and down-regulation of p

73 sistent with a pathway whereby PRC regulates NRF-2-dependent genes through a multiprotein complex inv

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

75 e mice with combined deficiency of NF-E2 and Nrf-2 did not exhibit a defect in erythroid maturation b

76 ion experiments with the authentic NRF-1 and NRF-2 DNA oligomers from previously characterized nuclea

77 Unlike the NRF-2 domain, which contains its essential hydrophobic m

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

79 tal liver cells deficient for both NF-E2 and Nrf-2 expressed normal levels of alpha- and beta-globin.

80 NaHS treatment increased Nrf-2 expression 1.8 times.

81 fucoxanthin treatment could restore PI3K/Akt/Nrf-2 expression in H(2)O(2)-treated PL-MSCs.

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

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

84 ear respiratory factor 2/GA binding protein (NRF-2/GABP), and ying-yang protein 1 (YY1).

85 this hypothesis for Nrf-2, we disrupted the Nrf-2 gene by homologous recombination.

86 stimulates a powerful induction of NRF-1 and NRF-2 gene expression; in addition, PGC-1 binds to and c

87 Nuclear respiratory factor 2 (NRF-2) has been shown to contribute to the transcription

88 Three members, p45-Nf-e2, Nrf-1 and Nrf-2 have been identified in mammals.

89 ion through dopaminergic neuroprotection via Nrf-2 HO-1 pathways.

90 estored antioxidant genes (p < 0.05) such as Nrf-2-HO-1, and prevented cardiac fibrosis in ISO-admini

91 O-administered rats, potentially through the Nrf-2-HO-1-mediated restoration of antioxidant enzymes a

92 We conclude that the Nrf-2/HO-1 axis is a critical pathway in the hyperglucid

93 utophagy were enhanced in TG(AC8) vs WT, and Nrf-2, Hsp90alpha, and ACC2 protein levels were increase

94 inhibitor PP2 caused nuclear accumulation of Nrf 2 in normal and hydrogen peroxide-treated cells but

95 Overexpression of Nrf-2 in astrocytes specifically increases expression of

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

97 These results suggest that local levels of NRF-2 in the monkey visual cortex closely reflect neuron

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

99 Once this is achieved, Nrf 2 is exported out of the nucleus, binds with INrf 2,

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

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

102 NRF-2 is of special significance because it co-regulates

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

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

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

106 , IL-1beta-stimulated chondrocytes had lower Nrf-2 levels in vitro, particularly in the nuclear fract

107 An important stress response is the Nrf-2 mediated oxidative stress response pathway where e

108 oxidative stress, astrocytes activate their Nrf-2-mediated thiol antioxidant defenses, promoting cel

109 in HG+IL-1beta-stimulated chondrocytes from Nrf-2(-/-) mice than in chondrocytes from wild-type mice

110 istribution of the alpha subunit proteins of NRF-2 (NRF-2 alpha) with CO in the monkey striate cortex

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

112 oxidative stress damage through the PI3K/Akt/Nrf-2 pathway.

113 ways (e.g., increased PGC1A gene expression, NRF-2 protein abundance, and phosphorylation of eIF2alph

114 ound for reciprocal upregulation of NF-E2 or Nrf-2 protein in fetal liver cells deficient for either

115 ingly, Nox4-deficient LECs exhibited reduced Nrf-2 protein level and deletion of Nox4 reduced Nrf-2 r

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

117 ith metformin in vivo, AMPK phosphorylation, NRF-2 protein, and PGC1A expression are increased.

118 icated that the -94 to -101 region binds the NRF-2 protein.

119 nsfection of dominant-negative constructs of NRF-2 proteins caused a significant reduction of COX exp

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

121 shares homology to the originally identified Nrf-2 recognition sequence, the two sequences are not id

122 r protein of Nrf-2 that, in combination with Nrf-2, regulates the polyamine analogue-induced transcri

123 2 protein level and deletion of Nox4 reduced Nrf-2 reporter gene activity.

124 suggest that increases in PGC-1, NRF-1, and NRF-2 represent key regulatory components of the stimula

125 and inhibit the antioxidant response element Nrf-2, resulting in depleted glutathione levels.

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

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

128 luding a GC box (Sp1-binding site) and three NRF-2 sites, one of which was located precisely beside t

129 equence-specific activators including NRF-1, NRF-2, Sp1, YY1, CREB and MEF-2/E-box factors, among oth

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

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

132 cumulation, activates Nrf-2, and upregulates Nrf-2 target gene expression in these astrocytes.

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

134 has been identified as a partner protein of Nrf-2 that, in combination with Nrf-2, regulates the pol

135 clone and identify the transcription factor, Nrf-2, that binds constitutively to the PRE sequence.

136 r 1 (NRF-1) to the cytochrome c promoter and NRF-2 to the cytochrome oxidase subunit 4 promoter incre

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

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

139 recruitment of nuclear respiratory factor 2 (NRF-2) to its target promoters, activating a subset of n

140 a third common factor, along with NRF-1 and NRF-2, to be associated with COX gene regulation.

141 The Nrf-2 transcription factor appears only to be present in

142 redox defenses by upregulating levels of the Nrf-2 transcription factor, as well its targets, the xCT

143 ptosis, and enhanced the accumulation of the Nrf-2 transcription factor.

144 Nrf 2 translocates to the nucleus binds to ARE and activ

145 Nuclear factor Nrf 2, under normal conditions, is retained in the cytos

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

147 The findings indicate that NRF-1 and NRF-2 utilize similar hydrophobic structural motifs for

148 To test this hypothesis for Nrf-2, we disrupted the Nrf-2 gene by homologous recombi

149 The activation domains of both NRF-1 and NRF-2 were extensively characterized by both deletion an

150 or the nuclear respiratory factors NRF-1 and NRF-2 were identified.

151 or the nuclear respiratory factors NRF-1 and NRF-2, which have been shown to contribute to the transc

152 ains two YY1 sites and at least one site for NRF-2, which show binding to their cognate factors.

153 tive association of the transcription factor Nrf-2 with the recently discovered polyamine-responsive