ライフサイエンスコーパス: AhR

1 AhR activation of LC by FICZ caused downregulation of Fc

2 AhR activation prevented the development of insulitis ca

3 AhR activity depends on its binding to the xenobiotic re

4 AhR binding to the NC-XRE in response to activation by t

5 AhR deficiency abolished the protective effects of gamma

6 AhR deficiency also impaired the in vivo differentiation

7 AhR depletion induces undifferentiation and pluripotency

8 AhR expression was increased in the heart of infected WT

9 AhR ligands can accelerate keratinocyte differentiation,

10 AhR overexpression further increased BCRP mRNA and prote

11 AhR was also found in keratinocytes, which lack AhRR.

12 AhR-deficient (Ahr(-/-)) B cells proliferate less than A

13 AhR-mediated regulation of FcepsilonRI did not involve a

14 AhR-null tumoral tissue, but not their surrounding non-t

15 ely, using a chicken PCR array comprising 27 AhR-related genes.

16 receptor (AhR), which bound to and activated AhR response elements in the Jag1 promoter.

17 ctivation properties of the ligand-activated AhR but did not affect its E3 ubiquitin ligase function.

18 We show that tapinarof binds and activates AhR in multiple cell types, including cells of the targe

19 n human placental trophoblasts by activating AhR.

20 ible population had a risk of the activating AhR pathway greater than that of adults.

21 ntrol (AhR(fl/fl)) mice but not in adipocyte AhR-deficient mice (AhR(AdQ)).

22 Our results demonstrate that adipocyte AhR mediates PCB-induced adipose inflammation and impair

23 olin-7-one (10-Cl-BBQ), a nanomolar affinity AhR ligand with immunosuppressive activity and favorable

24 amine (DEN) produced large carcinomas in all AhR-/- mice but mostly premalignant adenomas in less tha

25 PM activates an AhR-Jag1-Notch cascade to promote allergic airway inflam

26 mary, these studies identify tapinarof as an AhR agonist and confirm that its efficacy is dependent o

27 e that of SR1, appeared to be mediated by an AhR-dependent mechanism because both culture conditions

28 a1 (TGF-beta1) is induced by flutamide in an AhR-dependent manner.

29 to induce the CYP1A1 gene, thus revealing an AhR agonist-specific mutually exclusive dichotomous tran

30 stly associated with DNA modifications to an AhR pathway gene, the AhR repressor (AHRR).

31 uman dendritic cells (DC) associated with an AhR-dependent increase of CYP1A1 (cytochrome P4501A1).

32 nd transcription factors, cMaf, Blimp-1, and AhR.

33 We investigated AhR and AhR repressor (AhRR) expression and functional consequen

34 vertheless similarly expressed in AhR+/+ and AhR-/- lesions.

35 yl hydrocarbon receptor repressor (AhRR) and AhR-mediated induction of CYP1A1, cytokines, and acute t

36 ranscriptome comparison of AhR-deficient and AhR-sufficient B cells identified cyclin O (Ccno), a dir

37 We infected wild-type (WT) mice and AhR knockout (AhR KO) mice with T. cruzi (Y strain) and

38 studies, we investigated the role of MR and AhR in IDO regulation and its effect on T helper cell di

39 C) were treated with the UV photoproduct and AhR ligand 6-formylindolo[3,2-b]carbazole (FICZ).

40 POPs with high TEFs and AhR affinity were associated with longer LTL.

41 identified many barrier-associated genes as AhR targets.

42 Blockade of AhR using a clinically available AhR antagonist greatly enhanced the in vitro generation

43 by regulating Blimp-1 expression via Bach2, AhR represses differentiation of B cells into plasmablas

44 t mutants derived from the CLOCK:BMAL1-based AhR:ARNT dimer models of both the PAS-A and the PAS-B dr

45 a HF diet, both genotypes became obese, but AhR(AdQ) mice administered vehicle (VEH) exhibited incre

46 arget of AhR, as a top candidate affected by AhR deficiency.

47 ders multiciliogenesis and Ccno induction by AhR independent from air exposure.

48 )Foxp3(-)RORgammat(+) cells was inhibited by AhR activation.

49 e could show upregulation of IDO mediated by AhR engagement.

50 oly(ADP-ribose)polymerase (Tiparp/TiPARP) by AhR ligands were gene- and cell context-dependent with t

51 , air exposure does not induce the canonical AhR target cytochrome P450 1a1 (Cyp1a1).

52 In conclusion, AhR influences the development of murine Chagas disease

53 Experiments with conditionally AhR-deficient mouse lines identified keratinocytes as th

54 tolerance in LF (low fat diet)-fed control (AhR(fl/fl)) mice but not in adipocyte AhR-deficient mice

55 ate on enhancing induction of Cyp1b1/CYP1B1, AhR repressor (Ahrr/AhRR) and TCDD-inducible poly(ADP-ri

56 CA-dependent AhR-XRE-mediated Stc2 upregulation is responsible for cy

57 -p-dioxin (TCDD) and also microbiota-derived AhR ligands tryptamine, indole and 1,4-dihydroxy-2-napht

58 er model as the most suitable for describing AhR:ARNT dimerization.

59 sent study, we tested the ability of dietary AhR ligands (indole-3-carbinol [I3C] and 3,3'-diindolylm

60 T cell differentiation, and use of distinct AhR ligands has shown that whereas some ligands induce r

61 3'-diindolylmethane [DIM]) and an endogenous AhR ligand, 6-formylindolo(3,2-b)carbazole (FICZ), on th

62 ryptophan derivatives that act as endogenous AhR ligands can affect the transcription level of the ma

63 AhR target gene responsive to the endogenous AhR agonist cinnabarinic acid (CA).

64 er, our data demonstrate that the endogenous AhR ligand FICZ displays nanomolar photodynamic activity

65 rs Panobinostat and Vorinostat also enhanced AhR ligand-mediated induction and this was accompanied b

66 Butyrate synergistically enhanced AhR ligand-induced Cyp1a1/CYP1A1 in these cells with com

67 Upon hapten exposure, AhR(-/-) mice are not able to mount an NK cell memory re

68 Epidermal LC and CD34LC express AhR and AhRR.

69 s in the mouse liver, constitutively express AhR.

70 ptor signaling via the transcription factors AhR and RORgammat in T cells was necessary and sufficien

71 ation with a panel of activating ligands for AhR [2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)], CAR [6

72 ing that Foxp3(+) cells are not required for AhR-mediated suppression and furthermore that the AhR pa

73 ledge, the first demonstration of a role for AhR in the pathogenesis of malaria.

74 Thus, our data suggest a critical role for AhR in the regulation of inflammatory responses and open

75 ty, indicating that endogenous ligand(s) for AhR regulate adipose homeostasis.

76 ammatory properties of tapinarof derive from AhR agonism is conclusively demonstrated using the mouse

77 ike side population cells (SP) isolated from AhR-/- livers had increased beta-catenin (beta-Cat) sign

78 Our results suggest that functional AhR expression is critical for skin barrier integrity an

79 Here, AhR-null mice (AhR-/-) were used to explore whether AhR

80 ly 50 years of study, it remains unknown how AhR activation by dioxin produces toxic effects.

81 However, AhR function in these tissues is unknown.

82 Promoter analysis of the human AhR gene identified three putative NF-kappaB-binding ele

83 URI inhibits aryl hydrocarbon (AhR)- and estrogen receptor (ER)-mediated transcription

84 We have identified AhR as a novel target on donor T cells that is critical

85 Submersion and hypoxic conditions impede AhR-dependent Ccno induction.

86 In AhR(-/-) mice, there is a significant reduction in the p

87 n, and demyelination in EAE was abolished in AhR(-/-) mice.

88 The requirement for Foxp3(+) cells in AhR-induced suppression of insulitis was tested using NO

89 Therefore, flutamide may be effective in AhR-positive cancers that are sensitive to TGF-beta1 sig

90 NOG were nevertheless similarly expressed in AhR+/+ and AhR-/- lesions.

91 ameter of skin barrier integrity, is high in AhR-deficient mice.

92 ffect on TNF-alpha or glucose homeostasis in AhR(AdQ) mice exhibiting weight loss.

93 ct on imiquimod-induced skin inflammation in AhR-deficient mice.

94 ctivity in the epidermis of keratinocytes in AhR-knockout mice, and gene expression analysis identifi

95 ells only in wild-type (AhR(+/+)) but not in AhR knockout (AhR(-/-)) mice.

96 rm IDO expression in wild-type DC but not in AhR-deficient DC, establishing the central role of the k

97 ased during regeneration but more notably in AhR-null livers.

98 was earlier and more efficiently repaired in AhR-/- than in AhR+/+ mice.

99 OCT4 + and NANOG + cells expanded sooner in AhR-/- than in AhR+/+ regenerating livers.

100 more efficiently repaired in AhR-/- than in AhR+/+ mice.

101 OG + cells expanded sooner in AhR-/- than in AhR+/+ regenerating livers.

102 These drugs increased AhR recruitment onto the AhR-response elements and signi

103 lation is absolutely dependent on CA-induced AhR and MTA2 recruitment to the Stc2 regulatory region a

104 IDO enzymatic activity and IFN-gamma-induced AhR expression were required for continued IDO transcrip

105 , is AhR dependent, and air exposure induces AhR binding to the Ccno promoter.

106 on of a natural ligand of AhR, FICZ, induces AhR translocation to the nucleus and transcription of th

107 Infected AhR KO mice displayed significantly reduced parasitemia,

108 idative stress and activates an inflammatory AhR/p38MAPK/NF-kappaB pathway.

109 Interestingly, AhR and some components of the noncanonical nuclear fact

110 We investigated AhR and AhR repressor (AhRR) expression and functional c

111 cyclin O (Ccno) and Multicilin (Mcidas), is AhR dependent, and air exposure induces AhR binding to t

112 fected wild-type (WT) mice and AhR knockout (AhR KO) mice with T. cruzi (Y strain) and determined lev

113 ild-type (AhR(+/+)) but not in AhR knockout (AhR(-/-)) mice.

114 ablishing the central role of the kynurenine-AhR pathway in maintaining IDO expression in tolerogenic

115 We also show that CD4(+) T cells lacking AhR demonstrate reduced accumulation in secondary lympho

116 However, upon weight loss, AhR(fl/fl) mice administered PCB-77 exhibited increased

117 positively regulate IL-10 expression (MAFB, AhR), and promotes a proinflammatory state whose acquisi

118 at, as a downstream effector of 2AI-mediated AhR activation, palmitoleic acid protects RPE cells from

119 ice but not in adipocyte AhR-deficient mice (AhR(AdQ)).

120 Here, AhR-null mice (AhR-/-) were used to explore whether AhR controls liver

121 nds from the diet of wild-type mice mimicked AhR deficiency with respect to the impaired barrier; con

122 Moreover, AhR-deficient mice had higher interindividual difference

123 , a mutagenesis strategy for both the murine AhR and ARNT proteins was designed and ligand-dependent

124 ere we present homology models of the murine AhR:ARNT PAS domain dimer developed using recently avail

125 yl)-3-(1H-pyrrol-2-yl)acrylonitrile as a new AhR ligand.

126 CBs (composed of 10 non-dioxin-like PCBs; no AhR affinity and no TEF); b) non-ortho PCBs (composed of

127 ogether, 10-Cl-BBQ is an effective, nontoxic AhR ligand for the intervention of immune-mediated disea

128 chemical library screen to identify nontoxic AhR ligands with anti-cancer effects and discovered flut

129 Recent evidence identified a novel AhR DNA recognition sequence called the nonconsensus xen

130 identified stanniocalcin 2 (Stc2) as a novel AhR target gene responsive to the endogenous AhR agonist

131 , and three chemicals explained up to 71% of AhR activation.

132 edge for the first time, that the ability of AhR ligands to regulate the differentiation of Tregs ver

133 ay participate in the deleterious actions of AhR.

134 Activation of AhR by TCDD caused a significant increase of the inflamm

135 Pharmacologic antagonism of AhR or its lineage-specific deletion in CD11c(+) cells a

136 Blockade of AhR using a clinically available AhR antagonist greatly

137 Transcriptome comparison of AhR-deficient and AhR-sufficient B cells identified cycl

138 R) expression and functional consequences of AhR activation in human ex vivo skin cells and in in vit

139 We therefore tested the consequences of AhR activation in myelin oligodendrocyte glycoprotein (M

140 In this study, we tested the consequences of AhR activation in the NOD model.

141 licity, and the impact and considerations of AhR and CYP1A induction in the context of drug developme

142 318A mutations resulted in the conversion of AhR agonists beta-naphthoflavone and 3-methylcholanthren

143 Moreover, deficiency of AhR in adipocytes augmented the development of obesity,

144 one marrow chimeras we show that deletion of AhR in the immune system fully abrogates, whereas deleti

145 ese processes are likely to be downstream of AhR activation based on current evidence.

146 cell responses and represents an example of AhR's critical involvement in the regulation of allergic

147 y skin were analyzed for their expression of AhR and AhRR.

148 stimuli such as LPS induce the expression of AhR in human dendritic cells (DC) associated with an AhR

149 Basal expression of AhR, the AhR nuclear translocator, and the CYP1 family m

150 hance basal and ligand-induced expression of AhR-responsive genes.

151 ial inflammation and fibrosis, expression of AhR/cytokines/suppressor of cytokine signaling (SOCS) (s

152 unclear what the physiological functions of AhR in B cells are.

153 y premalignant adenomas in less than half of AhR+/+ mice.

154 processes, involving a complex interplay of AhR agonsim and saturation of metabolic machinery by com

155 nd IDO2) in DCs, with partial involvement of AhR.

156 UVA-induced oxidative stress irrespective of AhR ligand activity.

157 Knockdown of AhR by shRNA decreased BCRP expression, and this decreas

158 indole (2AI) as a potent synthetic ligand of AhR that protects RPE cells in vitro from lipid peroxida

159 Addition of a natural ligand of AhR, FICZ, induces AhR translocation to the nucleus and

160 in the samples accounted for the majority of AhR-mediated activity, PCDDs explained less than 5% of t

161 ould provide insights into the mechanisms of AhR transformation.

162 The relevance of AhR for the outcome of T. cruzi infection is not known a

163 Per-ARNT-SIM (PAS) protein, the repressor of AhR function (AhRR).

164 r, these data demonstrate the requirement of AhR for the maintenance of CD49a(+)TRAIL(+)CXCR6(+)DX5(-

165 We focus on the role of AhR in integrating signals from the diet and the intesti

166 To define the role of AhR in stroke, we used middle cerebral artery occlusion

167 yte differentiation, but the precise role of AhR in the skin barrier is unknown.

168 he emphasis is now shifting from the role of AhR in the xenobiotic pathway toward its mode of action

169 ession, indicating the ligand specificity of AhR activation.

170 endent of AR status, and that suppression of AhR expression reversed the anti-proliferative effects o

171 entified cyclin O (Ccno), a direct target of AhR, as a top candidate affected by AhR deficiency.

172 Topical treatment of AhR-sufficient mice with tapinarof leads to compound-dri

173 o discuss the potential therapeutic value of AhR agonists for multiple sclerosis and other autoimmune

174 differences in sensitivity to activation of AhRs (AhR1 and AhR2) can be predicted based on identitie

175 results from a cell-intrinsic dependence on AhR.

176 nd confirm that its efficacy is dependent on AhR.

177 inhibition or genetic attenuation of TDO2 or AhR increased cellular sensitivity to anoikis, and also

178 -TCDD that are lower than those of any other AhR of vertebrates tested to date.

179 Among three pathways, AhR was the most sensitive one activated by exposure to

180 rst time, that BUP, NBUP, and MET are potent AhR agonists and can induce BCRP in human placental trop

181 In contrast, the potent AhR agonist 2,3,7,8-Tetrachlorodibenzo-p-dioxin had no e

182 c end points mediated through a prototypical AhR ligand.

183 We tested the effect of the prototypical AhR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on

184 discovered flutamide (Eulexin) as a putative AhR ligand.

185 Here, we show that recipient mice receiving AhR(-/-) T cells have improved survival and decreased ac

186 inflammation, and aryl hydrocarbon receptor (AhR) activation and signaling may serve as a link betwee

187 Aryl hydrocarbon receptor (AhR) activation by high-affinity ligands mediates immuno

188 racterization and aryl hydrocarbon receptor (AhR) agonist activities of a series of chlorinated, brom

189 ty in response to aryl hydrocarbon receptor (AhR) agonist omeprazole and a 10-fold induction in respo

190 ous high-affinity aryl hydrocarbon receptor (AhR) agonist, acts as a nanomolar photosensitizer potent

191 uction through an aryl hydrocarbon receptor (AhR) and IL-23 receptor pathway.

192 s may bind to the aryl hydrocarbon receptor (AhR) and induce telomerase activity, which elongates LTL

193 Activation of aryl hydrocarbon receptor (AhR) and Nrf2-mediated oxidative stress response were fo

194 Aryl hydrocarbon receptor (AhR) has been shown to have profound influence on T cell

195 The aryl hydrocarbon receptor (AhR) has roles in cell proliferation, differentiation an

196 sequently for the aryl hydrocarbon receptor (AhR) in conversion.

197 The aryl hydrocarbon receptor (AhR) is a conserved, environmental ligand-dependent, per

198 The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor and a me

199 The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor involved

200 The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor involved

201 The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that aff

202 The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that is

203 The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that reg

204 The aryl hydrocarbon receptor (AhR) is a transcription factor modulated by exogenous an

205 The Aryl hydrocarbon Receptor (AhR) is a transcription factor that mediates the biochem

206 ental sensor, the aryl hydrocarbon receptor (AhR) is highly induced upon B cell activation and serves

207 The aryl hydrocarbon receptor (AhR) is involved in the regulation of immune responses,

208 Aryl hydrocarbon receptor (AhR) ligands are important for gastrointestinal health a

209 activation of the aryl hydrocarbon receptor (AhR) pathway and the subsequent induction of CYP1-metabo

210 activation of the aryl hydrocarbon receptor (AhR) pathway in laquinimod-treated mice.

211 s agonists of the aryl hydrocarbon receptor (AhR) pathway, and activation of the AhR pathway was show

212 known to repress aryl hydrocarbon receptor (AhR) signaling, but very little is known regarding the r

213 is independent of aryl hydrocarbon receptor (AhR) signaling.

214 antagonist of the aryl hydrocarbon receptor (AhR) transcription factor known to maintain CD34 express

215 activation of the aryl hydrocarbon receptor (AhR), a ligand activated transcription factor.

216 The aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor that respo

217 e response by the aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor whose acti

218 nterestingly, the aryl hydrocarbon receptor (AhR), a ligand-dependent transcription factor with an em

219 The aryl hydrocarbon receptor (AhR), a regulator of xenobiotic toxicity, is a member of

220 The aryl hydrocarbon receptor (AhR), a transcription factor known for mediating xenobio

221 activation of the aryl hydrocarbon receptor (AhR), activation of the pregnane X receptor (PXR), activ

222 cient to activate aryl hydrocarbon receptor (AhR), an endogenous kynurenine receptor.

223 Aryl hydrocarbon receptor (AhR), an important regulator of immune responses, is act

224 e receptor (CAR), aryl hydrocarbon receptor (AhR), and Nrf2.

225 nscription factor aryl-hydrocarbon receptor (AhR), compared to unprimed controls.

226 The aryl hydrocarbon receptor (AhR), for many years almost exclusively studied by the p

227 of activating the aryl hydrocarbon receptor (AhR), nuclear factor erythroid 2-related factor 2 (Nrf2)

228 s mediated by the aryl hydrocarbon receptor (AhR), which bound to and activated AhR response elements

229 cytokines via an aryl hydrocarbon receptor (AhR)-dependent mechanism.

230 in-A-induced IRF4-aryl hydrocarbon receptor (AhR)-dependent transcriptional network, which generates

231 d by CH223191, an aryl hydrocarbon receptor (AhR)-specific antagonist.

232 nscription factor aryl hydrocarbon receptor (AhR).

233 activation of the aryl hydrocarbon receptor (AhR).

234 activation of the aryl hydrocarbon receptor (AhR).

235 activation of the aryl hydrocarbon receptor (AhR).

236 matory nongenomic aryl hydrocarbon receptor (AhR)/p38MAPK/NF-kappaB pathway that induced the proinfla

237 genous ligands of aryl hydrocarbon receptor (AhR; a unique cellular chemical sensor).

238 act at adipocyte aryl hydrocarbon receptors (AhRs) to promote adipose inflammation and impair glucose

239 Interestingly, removing AhR ligands from the diet of wild-type mice mimicked AhR

240 , and this decrease was reversed by rescuing AhR expression.

241 These results demonstrate SCFA-AhR ligand interactions in YAMC and Caco-2 cells where S

242 ay represent a first-in-class drug targeting AhR for the treatment of multiple sclerosis and other ne

243 ent (Ahr(-/-)) B cells proliferate less than AhR-sufficient (Ahr(+/+)) cells following in vitro BCR s

244 critical for skin barrier integrity and that AhR represents a molecular target for the development of

245 We further demonstrate that AhR suppresses class switching in vivo after influenza v

246 We find that AhR negatively regulates class-switch recombination ex v

247 We found that AhR-knockout (KO) mice infected with P. berghei Anka dis

248 These data strongly support the idea that AhR is necessary for the efficacy of laquinimod in EAE a

249 These data indicate that AhR involvement in detoxification of environmental pollu

250 We also show that AhR has a causal role in acute ischemic damage because p

251 Here we show that AhR regulates multiciliogenesis in both murine airway ep

252 Our study shows that AhR activation by FICZ reduces FcepsilonRI and upregulat

253 Collectively, our data suggest that AhR activation promotes CPS1 recruitment to DNA enhancer

254 We suggest that AhR may serve to adjust liver repair and to block tumori

255 These experiments suggest that AhR serves as a molecular rheostat in B cells to brake t

256 The AhR is widely known as a mediator of dioxin toxicity; ho

257 The AhR pathway modulates the differentiation and function o

258 The AhR-KYN axis is potentially important in modulating mast

259 Basal expression of AhR, the AhR nuclear translocator, and the CYP1 family members do

260 eal a role of tryptophan derivatives and the AhR signalling pathway in regulating cancer cell stemnes

261 se by identifying an interaction between the AhR and the metastasis-associated protein 2 (MTA2).

262 -SIM (PAS) domains, is needed to convert the AhR into its transcriptionally active form, deciphering

263 anscriptionally active form, deciphering the AhR:ARNT dimerization mode would provide insights into t

264 ecently, endogenous regulatory roles for the AhR in normal physiology and development have also been

265 that TGF-beta1 induction is required for the AhR-dependent growth inhibitory effects of flutamide.

266 a potency measure including affinity for the AhR: a) non-dioxin-like PCBs (composed of 10 non-dioxin-

267 NA modifications to an AhR pathway gene, the AhR repressor (AHRR).

268 Historically, the AhR has been studied as a regulator of xenobiotic metabo

269 evealed a requirement of beta-catenin in the AhR-, CAR-, and PXR-mediated induction of CYP1A, CYP2B6

270 We investigated the AhR-dependent mechanism of action of flutamide in human

271 Moreover, the AhR-MTA2 interaction is CA-dependent and results in MTA2

272 ing a tumor-suppressive-like function of the AhR in MCF7 xenograft tumors.

273 eceptor (AhR) pathway, and activation of the AhR pathway was shown to promote atherosclerosis in mice

274 tion to the nucleus and transcription of the AhR target gene Cyp1a1, showing that the AhR pathway is

275 Among them, ITE enhances the binding of the AhR to the promoter of Oct4 and suppresses its transcrip

276 In addition, the activation of the AhR, Nrf2, and p53 pathways was compared by in vitro rep

277 ms underlying the functional activity of the AhR.

278 the modulation of the dual functions of the AhR.

279 ligand-dependent DNA binding ability of the AhR:ARNT heterodimer mutants was evaluated.

280 ese drugs increased AhR recruitment onto the AhR-response elements and significantly induced breast c

281 Recently, it was shown that the AhR has dual functions.

282 ediated suppression and furthermore that the AhR pathway is able to compensate for the absence of Fox

283 the AhR target gene Cyp1a1, showing that the AhR pathway is functional in B cells.

284 Furthermore, we demonstrated that the AhR-IDO pathway was responsible for the preferential act

285 molecular switch that determines whether the AhR acts as a transcription factor or an E3 ubiquitin li

286 Since dimerization with the AhR Nuclear Translocator (ARNT) protein, occurring throu

287 sponse element (XRE) in partnership with the AhR nuclear translocator (Arnt).

288 This AhR-mediated anti-inflammatory feedback mechanism may da

289 Thus, AhR might represent a novel molecular target for manipul

290 how allergens and lectins modulate the TLR4-AhR-IDO axis in human monocyte-derived DCs.

291 ey role for MR in the modulation of the TLR4-AhR-IDO axis, which has a significant effect on DC behav

292 r bile acid accumulation that contributes to AhR-mediated hepatotoxicity.

293 Inversely, exposure to AhR ligands induces Cyp1a1 but not Ccno and impeded cili

294 n of Tregs and Th17 cells only in wild-type (AhR(+/+)) but not in AhR knockout (AhR(-/-)) mice.

295 Unexpectedly, AhR(AdQ) mice exhibited increased fat mass when fed a st

296 tal autoimmune encephalomyelitis (EAE) using AhR knockout mice.

297 In vitro, AhR deficiency caused impairment in parasite replication

298 iltration without clinical toxicity, whereas AhR-deficient NOD mice were not protected.

299 l mice (AhR-/-) were used to explore whether AhR controls liver regeneration and carcinogenesis by re

300 and impaired glucose tolerance compared with AhR(fl/fl) controls.

301 in the colon of recipients transplanted with AhR(-/-) T cells 14 days after transplant.