ライフサイエンスコーパス: ARE

1 ARE-bound ATF5/p300 acetylates lysine-14 (K14) of nucleo

2 /Keap1 (Kelch-like ECH-associated protein 1)/ARE (antioxidant response element)-driven target gene sy

3 n)/Nrf2 (nuclear factor E2-related factor 2)/ARE (antioxidant response element) signaling system.

4 tes the important role of Nrf2 in activating ARE driven genes related to GSH metabolic pathway and al

5 (ChIP), which also indicated that the active ARE and RARE sites were adjacent, suggesting that the an

6 The incremental operative risk of adding ARE to AVR has not been established.

7 tabilization of VEGF mRNA was mediated by an ARE-like sequence in the proximal 3'UTR.

8 pressing Hsp70 in HeLa cells destabilized an ARE reporter mRNA, indicating a novel ARE-directed mRNA-

9 ology splicing regulatory protein (KSRP), an ARE-BP, is robustly up-regulated in human lung cancer.

10 ates TP53 mRNA stability through not only an ARE but also an adjacent miR-504/miR-125b-targeting site

11 Tis11 is thus an ARE-binding, mRNA-destabilizing protein that may play a

12 omains of Hsp70 could form complexes with an ARE sequence from VEGFA mRNA in vitro, only the peptide-

13 easured by aminophenyl fluorescein (APF) and ARE-FLuc luciferase assays, and ~45% cancer cell death a

14 the mVP24 K-Loop abrogates Kelch binding and ARE activation.

15 hat demonstrated activity in the ARE-bla and ARE-luc assays and were able to determine structural fea

16 g luciferase reporter driven by ARE-NQO1 and ARE-GST1 promoters.

17 A and androgen responsive elements (RARE and ARE) were mapped to the hTGP promoter by chromatin immun

18 uencing (ChIP-Seq) we refined AR-binding and AREs at a genome-scale in androgen-insensitive and andro

19 tabolism, and between harvested exudates and AREs, suggest that AREs are not chemically representativ

20 oach, we identified compound 7, a potent AR (ARE EC50 = 0.34 nM) and selective (N/C interaction EC50

21 of mRNAs containing AU-rich elements (AREs) (ARE-mRNAs).

22 element beta lactamase reporter gene assay (ARE-bla), which identifies chemicals that have the poten

23 In RNA decay assays, ARE(bcl-2) transcripts were protected from exosomal deca

24 und chaperone Hsp27 to be an AUF1-associated ARE-binding protein required for tumor necrosis factor a

25 Conversely, promoter mutated at ARE site did not respond to SFN, validating the SFN-medi

26 bition of dynamin-2 trapped rhodopsin-GFP at AREs and caused aberrant accumulation of coated vesicles

27 lia, with Rab11a regulating cargo sorting at AREs and carrier vesicle docking at the apical membrane.

28 Two putative atypical ARE half-sites are present at bp -200 and -827 (ARE1 and

29 atients with typical (n = 339) and atypical (ARE; n = 54) RE compared with the prevalence in 65,046 E

30 In-hospital mortality was higher after AVR+ARE (4.3% versus 3.0%, P=0.008), although when the cohor

31 ugust 2014, 7039 patients underwent AVR (AVR+ARE, n=1854; AVR, n=5185) at a single institution.

32 adjustment for baseline characteristics, AVR+ARE was not associated with an increased risk of in-hosp

33 rtality was not statistically different (AVR+ARE: 1.7% versus AVR: 1.1%, P=0.29).

34 Furthermore, AVR+ARE was not associated with an increased risk of postope

35 nderwent concomitant cardiac procedures (AVR+ARE: 68% versus AVR: 67%, P=0.31).

36 s slightly smaller in patients requiring AVR+ARE versus AVR (23.4+/-2.1 versus 24.1+/-2.3, P<0.001).

37 Patients undergoing AVR+ARE were more likely to be female (46% versus 34%, P<0.0

38 patients received bioprosthetic valves (AVR+ARE: 73.4% versus AVR: 73.3%, P=0.98) and also underwent

39 We utilized two cell-based ARE assay reporters, beta-lactamase and luciferase, to s

40 ntrast, relinquishes AR to permissively bind AREs across the genome, resulting in substantial AR-bind

41 uc) reporter gene based molecular biosensor (ARE-FLuc) to measure the antioxidant signaling response

42 onfirmed using luciferase reporter driven by ARE-NQO1 and ARE-GST1 promoters.

43 We classified AREs according to their degeneracy and their transcripti

44 A conserved ARE-related sequence was found in the EAAT3 promoter of

45 gene therapy in cells with high constitutive ARE activity, permitting a greater degree of therapeutic

46 oplasm and nucleus, binds to RNAs containing AREs, and promotes deadenylation of a model ARE transcri

47 t GAPDH binds with high affinity to the core ARE from tumor necrosis factor-alpha mRNA via a two-step

48 tep2 (= nETqe/(1 + ARECRE/AOECOE)) coulombs (ARE,AOE andCRE,COEare the areas (cm(2)) and differential

49 immunoprecipitation, we identified a crucial ARE motif within the MR 3'-UTR, to which Tis11b must bin

50 by proteasomes and stabilization of cytokine ARE-mRNAs.

51 zation of reporter mRNAs containing cytokine AREs.

52 In the largest analysis to date, ARE was not associated with increased risk of mortality

53 binding to an antioxidant response element (ARE) (-1286 to -1276) of the Txnip promoter.

54 ally important antioxidant response element (ARE) activation, and the resultant strength of ARE induc

55 7 targeted to the androgen response element (ARE) and the estrogen response element (ERE) were synthe

56 regulating the antioxidant response element (ARE) in response to oxidative stress and exposure to ele

57 placed from an antioxidant response element (ARE) in the gene promoter while Nrf2 is recruited to the

58 We identify an androgen response element (ARE) in the Hand2 locus and present biochemical evidence

59 The androgen response element (ARE) is a palindromic, dihexameric motif present in prom

60 of MafG to the antioxidant response element (ARE) of GCLC but lower Nrf2/MafG heterodimer binding to

61 ectable at the antioxidant response element (ARE) of several NFE2L2-responsive genes.

62 on of the NRF2-antioxidant response element (ARE) pathway.

63 5/p300 complex to the ATF5 response element (ARE) region of the Egr-1 promoter.

64 actor 2 (Nrf2)-antioxidant response element (ARE) regulates intracellular antioxidative capacity to c

65 igher antioxidative stress response element (ARE) reporter activity.

66 ctor-dependent antioxidant response element (ARE) signaling is activated by selective electrophilic m

67 The antioxidant response element (ARE) signaling pathway plays an important role in the am

68 identified an antioxidant response element (ARE) that is required for DJ-1-dependent induction of Tr

69 easured by the antioxidant response element (ARE) using a luciferase reporter, and induced Nrf2-media

70 regulation of antioxidant response element (ARE), a cis-acting enhancer sequence that binds Nrf2.

71 actor 2 (Nrf2)/antioxidant response element (ARE), which play an important role in antioxidant defens

72 f NRF2 and the antioxidant response element (ARE)-mediated transcription in an NRF2-dependent manner.

73 ed through the antioxidant response element (ARE)-nuclear factor erythroid 2-related factor 2 (Nrf2)

74 control of the antioxidant response element (ARE).

75 1 (NQO1) gene antioxidant response element (ARE).

76 carrying an antioxidant responsive element (ARE) after down-regulation of caveolin-1 by small interf

77 SA promoter and androgen-responsive element (ARE) luciferase activity.

78 tor 2 (Nrf2)-antioxidant responsive element (ARE) pathway by oxidative stress promotes astrocyte rele

79 ress via the antioxidant responsive element (ARE), to which nuclear factor-E2-related factor 2 (Nrf2)

80 tial for the antioxidant responsive element (ARE)-mediated expression of a group of detoxifying antio

81 An AU-rich element (ARE) and its cognate RNA-binding protein, HuR, were requ

82 s of this complex to be the AU-rich element (ARE) binding proteins AUF1 and HuR.

83 ired for the degradation of AU-rich element (ARE) containing messenger RNAs (mRNAs).

84 he existence of a conserved AU-rich element (ARE) in the 3'-untranslated region (UTR) of AChR beta-su

85 nscript are regulated by an AU-rich element (ARE) in the 3'-UTR of messenger RNA.

86 We found a conserved AU-rich element (ARE) in the human LARP4 mRNA 3' untranslated region (UTR

87 ' untranslated region (UTR) AU-rich element (ARE) motifs.

88 ivation of adenylate-uridylate-rich element (ARE)-binding protein BRF1, a target of PI3K-Akt.

89 AUF1 is an AU-rich element (ARE)-binding protein that recruits translation initiatio

90 ole of the adenine and uridine-rich element (ARE)-binding protein tristetraprolin (TTP) in influencin

91 The destabilization of AU-rich element (ARE)-containing mRNAs mediated by proteins of the TIS11

92 IFN-gamma adenylate-uridylate-rich element (ARE)-deleted (del) mice, which constitutively express a

93 his polymorphism influenced AU-rich element (ARE)-mediated decay (AMD) of IFNL3 mRNA, as well as the

94 AMP 3'-UTR harbors a single AU-rich element (ARE).

95 is mediated by androgen-responsive elements (ARE) and dictated by Polycomb group protein EZH2 and rep

96 emonstrate that cis-acting AU-rich elements (ARE) present within a 38-base pair region of the PIM1 mR

97 to transcripts containing AU-rich elements (ARE), resulting in deadenylation and destabilization of

98 Defects in AU-rich elements (ARE)-mediated posttranscriptional control can lead to se

99 ) through antioxidant response cis-elements (AREs) and are impaired in the aging heart.

100 al transcripts contain AU-rich cis-elements (AREs) recognized by tristetraprolin (TTP/Zfp36), an RNA-

101 how has three antioxidant response elements (AREs) in its promoter region, is strongly induced by Nrf

102 ously identified androgen response elements (AREs) in the HBV genome could indeed mediate the effect

103 nd binding to antioxidant response elements (AREs) in their gene promoter regions.

104 ng of Nrf2 to antioxidant response elements (AREs) or electrophile response elements (EpREs) in the 5

105 al high-affinity androgen response elements (AREs) that are preferentially engaged by AR, albeit with

106 xpression via antioxidant response elements (AREs), but their roles in embryonic development are not

107 genes bearing antioxidant-response elements (AREs).

108 atin through the androgen response elements (AREs).

109 genes through antioxidant response elements (AREs).

110 zation of mRNAs containing AU-rich elements (AREs) (ARE-mRNAs).

111 ry elements, which include AU-rich elements (AREs) and microRNA (miRNA) targeting sites, within the 3

112 dation of mRNAs containing AU-rich elements (AREs) at the 3' untranslated regions.

113 mbles mRNPs containing the AU-rich elements (AREs) bound by HuR proteins in a nondegradative, ubiquit

114 The AU-rich elements (AREs) encoded within many mRNA 3' untranslated regions (

115 ins (AUBPs) that recognize AU-rich elements (AREs) found within many transcripts.

116 s to numerous adenine-uridine rich elements (AREs) from various mRNA 3'-untranslated regions in vitro

117 oteins can bind to certain AU-rich elements (AREs) in mRNAs, leading to their deadenylation and desta

118 tly unstable mRNAs contain AU-rich elements (AREs) in the 3' untranslated regions.

119 binds to adenylate-uridylate-rich elements (AREs) in the 3'-untranslated regions (3'UTRs) of specifi

120 AU-rich elements (AREs) in the 3'-UTR of unstable transcripts play a vital

121 over contain destabilizing AU-rich elements (AREs) in their 3' untranslated regions.

122 mRNAs by first binding to AU-rich elements (AREs) in their 3'-untranslated regions (UTRs) and subseq

123 s have a higher density of AU-rich elements (AREs) in their 3'UTR and upstream open reading frames (u

124 ty of key mRNAs containing AU rich elements (AREs) known to be associated with glaucoma progression,

125 altered by the presence of AU-rich elements (AREs) located in the 3'-untranslated regions (3'UTRs) of

126 ch as the adenylate-uridylate-rich elements (AREs) present in the 3' untranslated region (UTR) of mRN

127 he TNF transcript contains AU-rich elements (AREs) that are targeted by the RNA-binding protein, tris

128 U-rich RNA including some AU-rich elements (AREs) that regulate the decay kinetics of select mRNAs a

129 code proteins that bind to AU-rich elements (AREs) within the 3' untranslated regions (3'UTRs) of man

130 e the GILZ 3'-UTR contains AU-rich elements (AREs), we analyzed the role of the mRNA-binding protein

131 conserved adenylate/uridylate-rich elements (AREs), were cloned downstream of a reporter gene.

132 Hsp70 also bound and stabilized endogenous ARE-containing mRNAs encoding vascular endothelial growt

133 -positive 'autophagy-related endomembranes' (ARE).

134 l Rab11-positive apical recycling endosomes (ARE) and reaches the apical membrane in a microtubule- a

135 its transfer to apical recycling endosomes (ARE) mediated by the plus-end kinesin KIF16B and non-cen

136 traffics through apical recycling endosomes (AREs) that bear the small GTPase Rab11a before arriving

137 proteins and suggest that Zfand5 can enhance ARE-containing mRNA stability by competing with tristetr

138 Surgical aortic root enlargement (ARE) during aortic valve replacement (AVR) allows for la

139 grown plants, and artificial root exudates (AREs) were created using a literature recipe.

140 ociation mechanisms of each AUF1 isoform for ARE-containing RNA substrates and quantified relevant bi

141 (KSRP), an RNA-binding protein required for ARE-mediated mRNA decay, produce higher levels of Ifna a

142 the scission of apical carrier vesicles from AREs.

143 bserved in wild-type recipients of IFN-gamma ARE-del BM.

144 reservoirs that retain AR via abundant half-AREs, thereby reducing its availability for specific sit

145 mental in recruiting AR to low-affinity half-AREs by opening local chromatin around adjacent FKHD sit

146 evidence that AR can directly bind the Hand2 ARE.

147 yocilin, SPARC, and MMP-3, which do not have AREs, were more stable after actinomycin D treatment and

148 to caveolin-1 (Phi-->A-Nrf2) hyperactivates ARE and inhibits oxidative stress-induced activation of

149 otein known to bind and destabilize class II ARE-containing RNAs.

150 ived from the androgen response element III (ARE III), which is required for the interaction of AR an

151 Although imperfect AREs make up 99.9% of the motifs, the degree of degenera

152 d in zebrafish induce a specific increase in ARE mRNAs encoding myelin proteins, showing that the imb

153 d decrease in Nrf2 ARE binding and increased ARE-dependent promoter activity, whereas combined knockd

154 oaches for identifying compounds that induce ARE signaling.

155 nal epithelial cells with TGF-beta inhibited ARE-mRNA expression.

156 Isoliquiritigenin and sulforaphane, known ARE activators that target Keap1, were used to validate

157 of lung cancer, suicide gene therapy with LV-ARE-TK/GCV was effective compared with LV-PGK-TK/GCV in

158 cid induces a switch from Nrf2 to c-Maf/MafG ARE nuclear binding, which leads to decreased expression

159 HuR expression led to changes in the mitosis ARE-mRNAs.

160 d correlated with high levels of the mitotic ARE-mRNA signature.

161 AREs, and promotes deadenylation of a model ARE transcript in a cell-based co-transfection assay.

162 phorylation controls AUF1 levels to modulate ARE mRNA degradation.

163 helial response by associating with multiple ARE-bearing, functionally related inflammatory transcrip

164 onal follow-up assay that employed a mutated ARE linked to beta-lactamase.

165 ancy enhances AR and FOXA1 binding to nearby ARE and FKHD sites, respectively.

166 roteasome subunit genes, however, contain no ARE/EpRE elements, and Nrf2 inducers, inhibitors, and si

167 s response for known liver toxicants when no ARE-bla data were available.

168 tion proximal to the ARE, but not to the non-ARE regions of ferritin genes.

169 s over-represented in cancer and, unlike non-ARE-mRNAs, correlated with the reversed balance in the e

170 zed an ARE reporter mRNA, indicating a novel ARE-directed mRNA-stabilizing role for this protein.

171 To identify novel ARE-dependent gene regulators, we screened a human leuko

172 lly blunted the LCA-induced decrease in Nrf2 ARE binding and increased ARE-dependent promoter activit

173 ct of tert-butylhydroquinone (tBHQ), an Nrf2-ARE signaling pathway inducer, on mitochondrial function

174 pathways-including hypoxia, metabolism, NRF2-ARE, Hippo, and immune checkpoint-can further distinguis

175 gnals, promoting comparable strength of Nrf2-ARE induction.

176 veral redox-sensitive regulators of the Nrf2-ARE axis.

177 cific regulation of the Shc gene by the Nrf2-ARE pathway and a new antioxidant role of p66Shc in the

178 Chemical activation of the Nrf2-ARE pathway in mouse brain increased both neuronal EAAT3

179 ated with type 1, and activation of the NRF2-ARE pathway was associated with type 2; CDKN2A loss and

180 ronal cysteine transporter EAAT3 by the Nrf2-ARE pathway.

181 ch was directly correlated to decreased Nrf2/ARE binding.

182 demonstrated a progressive reduction in Nrf2/ARE binding (-357/-349) of Prdx6 promoter.

183 aluated them as activators of the Keap1/Nrf2/ARE pathway and inhibitors of iNOS.

184 and their potency to activate the Keap1/Nrf2/ARE pathway was evaluated.

185 blasts to show that the upregulation of Nrf2/ARE genes by MB is Nrf2 dependent and not due to seconda

186 The activation of Nrf2/ARE genes is neuroprotective in other transgenic mouse m

187 with SFN's dose-dependent activation of Nrf2/ARE interaction.

188 idating the SFN-mediated restoration of Nrf2/ARE signaling.

189 mportant for the transcriptional activity of ARE-driven genes HO1 and NAD(P)H:quinine oxidoreductase

190 Here, we performed a systematic analysis of ARE-mRNA expression across multiple cancer types.

191 evealed that AtTZF1 can trigger the decay of ARE-containing mRNAs in vivo.

192 (i) The rates of degradation of ARE mRNA at early times (3 h) after infection with the w

193 Hence the rapid degradation of ARE mRNAs noted in DeltaICP27 mutant-infected cells at l

194 the TIS11 family, induces the degradation of ARE-containing mRNAs through a large variety of mechanis

195 , partially through the dephosphorylation of ARE-binding protein BRF1.

196 that Tis11 could promote destabilization of ARE-containing mRNAs and that this was partially depende

197 hat loss of Prdx6 caused by dysregulation of ARE/Nrf2 can be attenuated through a SFN, to combat dise

198 e further demonstrate that the efficiency of ARE-dependent mRNA degradation declines in the neural li

199 fand5 in macrophages decreased expression of ARE class II transcripts TNF and COX2, whereas overexpre

200 Expression of ARE-containing type I interferon transcripts is robustly

201 ells revealed that Myc regulates hundreds of ARE-containing (ARED) genes and select AUBPs.

202 tor 2 (Nrf2), which is a critical inducer of ARE-mediated expression, is regulated by DJ-1.

203 n contrast, the transcriptional influence of ARE half sites can be modulated by cooperating factors.

204 effect of PA, suggesting the involvement of ARE-binding proteins.

205 th an approximately 50% shorter half-life of ARE-containing transcripts.

206 dTIS11 does not promote the localization of ARE-containing mRNAs in P-bodies but rather decreases th

207 ut the role of shuttling in the mechanism of ARE-dependent mRNA decay.

208 erved family of proteins in the mechanism of ARE-mediated mRNA decay.

209 However, the role of ARE-BPs in lung cancer remains poorly understood.

210 A large set of ARE-mRNAs was over-represented in cancer and, unlike non

211 E) activation, and the resultant strength of ARE induction recapitulates that observed from whole-cel

212 has been shown to promote the translation of ARE-containing mRNAs.

213 porter assays confirmed the functionality of AREs.

214 se results significantly broaden the role of AREs and their binding proteins in cancer, and demonstra

215 esults provide direct evidence for a role of AREs as a post-Golgi sorting hub in the biosynthetic rou

216 this regulatory loop by modeling the role of AREs in mediating the messenger RNA stability and transl

217 onship (QSAR) models were developed based on ARE-bla data.

218 ed c-Met-dependent ERK1/2 phosphorylation on ARE.

219 grin-dependent c-Met-sustained signalling on ARE supports anchorage-independent cell survival and gro

220 aberrant accumulation of coated vesicles on AREs, suggesting a previously unrecognized role for dyna

221 Here, we present evidence that not only ARE- but also miRNA-mediated pathways are involved in PA

222 r protein that binds to AU-rich elements, or AREs, in the 3' noncoding regions (NCRs) of mRNAs to aff

223 ced in conjunction with suppression of other ARE-dependent antioxidant genes.

224 but not its RNA binding mutant or the other ARE-binding proteins tested, decreased cellular LARP4 le

225 ing identified a cluster of 11 overexpressed ARE-mRNAs (CDC6, KIF11, PRC1, NEK2, NCAPG, CENPA, NUF2,

226 which Nrf2 is constitutively overexpressed, ARE activity was found to be high under basal conditions

227 Weaker AREs, particularly ARE half sites, benefit from neighboring motifs or coope

228 estruction by proteasomes, thereby promoting ARE mRNA stabilization.

229 AU-rich element-binding proteins (ARE-BPs) offer post-transcriptional regulation of gene e

230 Additionally, we quantified ARE utilization in response to somatic copy number ampli

231 nt of rare variants in the GABRG2 gene in RE/ARE patients (5 of 204, 2.45%) in comparison to controls

232 the GABRG2 gene may increase the risk of RE/ARE.

233 AA -R genes in 204 European patients with RE/ARE versus 728 platform-matched controls.

234 in a proteasome-dependent fashion and render ARE mRNAs more stable.

235 ic mutant forms of Hsp27 stabilizes reporter ARE mRNAs.

236 of the MDM2 protein bound to the MYCN mRNA's AREs within the 3'UTR and increased MYCN 3'UTR-mediated

237 at the binding and stabilization of selected ARE-containing mRNAs may contribute to the cytoprotectiv

238 In this setting, ARE-HSV-TK was more effective than a vector in which HSV

239 n and IL23p19 mRNA stability through several AREs in the 3' untranslated region.

240 cently been shown to bind and stabilize some ARE-containing transcripts in cells.

241 imetic mutant forms of Hsp27 also stabilizes ARE-mRNAs.

242 support the hypothesis that ICP27 stabilizes ARE mRNAs.

243 Activating either kinase stabilizes ARE mRNAs.

244 ell electrophile flooding fails to stimulate ARE induction prior to causing cytotoxicity.

245 2 accumulation in the nucleus and subsequent ARE activation.

246 TG5 and Beclin1 but not on ATG13, suggesting ARE belong to a non-canonical autophagy pathway.

247 Surgical ARE is a safe adjunct to AVR in the modern era.

248 We conclude that ARE-regulated HSV-TK/GCV therapy offers a promising appr

249 en harvested exudates and AREs, suggest that AREs are not chemically representative of plant root exu

250 The ARE-binding protein human antigen R (HuR) stabilizes mRN

251 The ARE-bla computational model and HTS data from a big data

252 ctivity of a luciferase reporter bearing the ARE sequence from TNF (ARE(TNF)).

253 (K14) of nucleosomal histone H3 at both the ARE and serum response element (SRE) of the Egr-1 promot

254 o TP53 mRNA, and that can be reverted by the ARE-binding protein HuR.

255 The liver toxicants profile contained the ARE-bla and relevant PubChem assays.

256 First, the ARE database (ARED) was intersected with The Cancer Geno

257 compounds that demonstrated activity in the ARE-bla and ARE-luc assays and were able to determine st

258 scription and protein levels for most of the ARE-antioxidants were increased in young mice but their

259 ormation, TGF-beta induced expression of the ARE-binding protein tristetraprolin (TTP), which colocal

260 F2-modulated transcriptional activity of the ARE-driven genes, HO1 and NQO1.

261 his function by promoting degradation of the ARE-mRNA decay factor AUF1 by proteasomes.

262 RNA-IP demonstrated the association of the ARE-mRNAs with TTP and HuR.

263 allowing for expansion and refinement of the ARE.

264 ucleus and enhances its recruitment onto the ARE site in the Trx1 promoter.

265 Collectively, PRMT1 and PRMT4 regulate the ARE and cellular antioxidant response to arsenic.

266 We hypothesized that the ARE-bearing GATA-3 gene, a critical regulator of Th2 pol

267 Experimentally, we demonstrated that the ARE-mRNA cluster is upregulated in a number of tumor bre

268 tation showed that RAC3 bound tightly to the ARE enhancer region of the HO-1 promoter via Nrf2 bindin

269 perones, and mRNA degradation enzymes to the ARE for mRNA destruction.

270 e H4R3 and H3R17 methylation proximal to the ARE, but not to the non-ARE regions of ferritin genes.

271 gene promoter while Nrf2 is recruited to the ARE.

272 t lower Nrf2/MafG heterodimer binding to the ARE.

273 ure activated ferritin transcription via the ARE concomitant with increased methylation of histones H

274 By mutagenesis of the AREs within the CTH2 transcript, we demonstrate that a C

275 cumulation but inhibited Nrf2 binding to the AREs by approximately 40% (P<0.05), thus diminishing fer

276 How GAPDH binds to these AREs is still unknown.

277 This ARE, but not its antisense version or a point-mutated ve

278 This ARE-related sequence was bound by Nrf2 in mouse neurons

279 Mutation of this ARE abolished the effect of PA, suggesting the involveme

280 By contrast, mutation of this ARE prevented this increase.

281 reporter bearing the ARE sequence from TNF (ARE(TNF)).

282 et tissue levels of RA remained lower in TNF+ARE than wild-type mice, indicating that epithelial up-r

283 inant Drosophila Tis11 protein could bind to ARE-containing RNA oligonucleotides with low nanomolar a

284 fG by SUMO-1, which promoted Nrf2 binding to ARE and heterodimerization with MafG.

285 of AUF1p45 to TTP potentiated TTP binding to ARE-containing RNA probes, as determined by RNA gel shif

286 but higher Nrf2/MafG heterodimer binding to ARE.

287 A transacting protein, TTP, binds to ARE and enhances the mRNA turnover.

288 Zfand5 specifically bound to ARE(TNF) mRNA and competed with tristetraprolin, a prote

289 Binding of Nrf2 to ARE also suppressed the binding of MondoA to the carbohy

290 bility of the full-length protein to bind to AREs within the tumor necrosis factor alpha (TNF) mRNA 3

291 d Cth2 proteins specifically bind in vivo to AREs located at the 3'UTRs of their own transcripts in a

292 Taken together, ARE full sites generate a reliable transcriptional outco

293 lected 50 compounds for retesting in the two ARE assays and in an additional follow-up assay that emp

294 Weaker AREs, particularly ARE half sites, benefit from neighbor

295 cytoplasmic RNA processing (P) bodies where ARE-mRNA localization was observed.

296 The promoter (-918) with ARE showed a marked reduction in young vs aged hLECs, wh

297 70 form direct, high-affinity complexes with ARE substrates based on specific recognition of U-rich s

298 olding properties, is known to interact with ARE-like RNA substrates in vitro.

299 bilizes mRNA through direct interaction with AREs on 3'-UTR.

300 of Ifna4 and Ifnb mRNAs by interaction with AREs.

301 s of patients undergoing AVR with or without ARE.