ライフサイエンスコーパス: ARE

1 ARE disruption also results in constitutive phosphoinosi

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

3 ar factor [erythroid-derived 2]-like 2) to 2 AREs (antioxidant response elements) in the proximal IL1

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

19 ed as destabilizing motifs, with miR-430 and AREs causing mRNA deadenylation upon genome activation.

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

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

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

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

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

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 eracts this effect, as shown in a cell-based ARE reporter assay and by qPCR with native HuR mRNA targ

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

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

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

44 AUF1 then targets checkpoint ARE-mRNAs for degradation, progressively reprogramming t

45 We classified AREs according to their degeneracy and their transcripti

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

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

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

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

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

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

52 by proteasomes and stabilization of cytokine ARE-mRNAs.

53 zation of reporter mRNAs containing cytokine AREs.

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

55 nd non-phosphorylatable TTP mutant decreases ARE-bearing TNFalpha and DUSP1 mRNAs and sensitizes leuk

56 crystal structure of RRM3 bound to different ARE motifs.

57 while decay of AU-rich instability element (ARE)-signal containing mRNAs are not affected.

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

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

60 7 targeted to the androgen response element (ARE) and the estrogen response element (ERE) were synthe

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

77 1 (NQO1) gene antioxidant response element (ARE).

78 control of the antioxidant response element (ARE).

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

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

81 ecruited to the androgen responsive element (ARE) sequences on the DNA where AR interaction with coac

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

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

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

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

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

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

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

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

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 d in a subset of androgen response elements (ARE).

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

97 conserved adenylate-uridylate-rich elements (ARE) located in 3'untranslated regions (UTR) to mediate

98 UTR, which is dependent on AU-rich elements (ARE) present in the Sox2 mRNA 3'UTR.

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

100 target sequences, UAUUUAUU AU-rich elements (ARE), CCUC, and CUGC elements emerged as destabilizing m

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

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

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

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

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

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

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

108 es containing antioxidant-response elements (AREs) in their promoter regions.

109 2 activity on antioxidant response elements (AREs) localized to a microtubule-associated protein (Map

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

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

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

113 atin through the androgen response elements (AREs).

114 genes through antioxidant response elements (AREs).

115 genes bearing antioxidant-response elements (AREs).

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

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

118 ylation of RNAs containing AU-rich elements (AREs) and Pumilio-response elements (PREs).

119 Importantly, AU-rich elements (AREs) are significantly enriched in the upregulated G0 t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

138 ntranslated region (3'UTR) AU-rich elements (AREs).

139 e/uridylate-rich elements (AU-rich elements; AREs).

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

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

142 tions disrupt the apical recycling endosome (ARE) and membrane traffic, resulting in reduced surface

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

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

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

146 e to isolate HE and aortic roof endothelium (ARE)s, excluding non-aortic endothelium.

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

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

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

150 the scission of apical carrier vesicles from AREs.

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

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

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

154 evidence that AR can directly bind the Hand2 ARE.

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

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

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

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

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

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

161 oaches for identifying compounds that induce ARE signaling.

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

163 Surprisingly, currently known ARE ABCFs are not confined to a distinct lineage of the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

199 This permits expression of ARE mRNAs that promote chemoresistance.

200 TTP axis as a key regulator of expression of ARE-bearing mRNAs that promote chemoresistance.

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

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

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

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

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

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

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

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

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

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

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

212 porter assays confirmed the functionality of AREs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

231 Although all NRF members regulate ARE-containing genes, each is associated with distinct r

232 d loci are enriched for sequences resembling ARE half-sites that match the Py-Im polyamide binding pr

233 and the evolution of antibiotic resistance (ARE) factors from other ABCFs have not been explored.

234 ulture assays revealed the mechanism of RRM3 ARE recognition and dimerization.

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

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

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

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

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

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

241 Finally, although HuR stabilizes ARE-containing RNAs, we found that RRM3 counteracts this

242 ve p38 MAPK-MK2 signaling pathway stabilizes ARE mRNAs by phosphorylation and inactivation of mRNA de

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

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

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

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

247 age of the ABCF family tree, suggesting that ARE can readily evolve from other ABCF functions.

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

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

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

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

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

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

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

255 egulin led to dissociation of SLIRP from the ARE.

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

257 Comparatively, permutations of the ARE half-site bearing single or double mismatches to the

258 Analysis of the ARE motifs identified in ChIP peaks revealed that NRF2 p

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

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

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

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

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

269 gene promoter while Nrf2 is recruited to the ARE.

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

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

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

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

274 How GAPDH binds to these AREs is still unknown.

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

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

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

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

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

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

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

282 but higher Nrf2/MafG heterodimer binding to ARE.

283 SLIRP was bound to ARE's of AR target genes in the absence of androgen.

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

285 resses arterial markers at similar levels to ARE.

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

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

288 peaks revealed that NRF2 prefers binding to AREs flanked by GC-rich regions and that NRF1 prefers AT

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

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

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

292 here are a number of previously unidentified ARE ABCFs in antibiotic producers and important human pa

293 Further, we demonstrate that Sox2 3'UTR AREs are necessary for RBM24-based elevation of Sox2 mRN

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 s of patients undergoing AVR with or without ARE.