ライフサイエンスコーパス: AhR

1 AhR activation by indoxyl sulfate, a uremic toxin, leads

2 AhR activation of LC by FICZ caused downregulation of Fc

3 AhR activity depends on its binding to the xenobiotic re

4 AhR deficiency abolished the protective effects of gamma

5 AhR deficiency also impaired the in vivo differentiation

6 AhR deficiency reversed PCB-77-induced glucose impairmen

7 AhR depletion induces undifferentiation and pluripotency

8 AhR inhibitors exert significant antitumor activity and

9 AhR is important for modulation of the host immune respo

10 AhR ligands include diverse compounds from environmental

11 AhR overexpression further increased BCRP mRNA and prote

12 AhR sensing of TB drugs modulates host defense mechanism

13 AhR signalling, in turn, ensures on-demand production of

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

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

16 AhR-deficient females (VEH) were resistant to diet-induc

17 AhR-mediated regulation of FcepsilonRI did not involve a

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

19 AhR-ROR-gammat complex is a therapeutic target for MAP4K

20 AhR; Aryl hydrocarbon receptor.

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

22 the existence of a functional 5-HT/5-HT(2B)/AhR axis in human macrophages and indicate that 5-HT pot

23 pigment, the naphthoquinone Lawsone activate AhR, both in vitro and in vivo.

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

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

26 n human placental trophoblasts by activating AhR.

27 und that chemically inhibiting or activating AhR reciprocally modulated the expression levels of cyto

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

29 ek 11) and loss (week 15); liver and adipose AhR and IRS2 (insulin receptor substrate 2) mRNA abundan

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

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

32 an apparent K(D) of 50 nm and behaves as an AhR antagonist.

33 We assigned mice to a conventional diet, an AhR ligand-free diet, or an AhR ligand-free diet supplem

34 roid progenitors and that it may do so in an AhR-dependent fashion.

35 ntional diet, an AhR ligand-free diet, or an AhR ligand-free diet supplemented with the dietary AhR l

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

37 the aryl hydrocarbon receptor (AhR)(6), and AhR-mediated signalling in ILC3 and gammadelta T cells c

38 ale mice responded differently to PCB-77 and AhR deficiency in body weight (BW) regulation and glucos

39 rfin, that inhibited GLK kinase activity and AhR-ROR-gammat interaction.

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

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

42 T cell infiltrate includes CCR6(+)CD4(+) and AhR(+)CD4(+) T cells with potential for plasticity to Th

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

44 ctively, the GLK-induced AhR-ROR-gammat (and AhR-phosphorylated ROR-gammat) complex is a therapeutic

45 phosphorylation and the AhR-ROR-gammat (and AhR-phosphorylated ROR-gammat) complex.

46 is transcriptional regulation of the IFN and AhR pathways by Tet1 was also present in human bronchial

47 ammation by direct regulation of the IFN and AhR pathways.

48 We also demonstrated changes in NOTCH1 and AhR expression of epidermis treated with coarse air PM.

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

50 hysiological conditions regulated by PXR and AhR.

51 Pregnane X receptor (PXR) and AhR-mediated activities were the most commonly detected.

52 ptive immunity to promote tumorigenesis, and AhR predicts the response to immunotherapy and represent

53 model of BRCA1-related BC, cancer-associated AhR and AREG control tumor growth and production of chem

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

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

56 Our studies indicate that B12 and FA bind AhR directly as competitive antagonists, blocking AhR nu

57 of evidence demonstrate that ezutromid binds AhR with an apparent K(D) of 50 nm and behaves as an AhR

58 irectly as competitive antagonists, blocking AhR nuclear localization, XRE binding, and target gene i

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

60 ainst challenge to their genome integrity by AhR-mediated 'sensing' of genotoxic compounds from the d

61 nding, and target gene induction mediated by AhR agonists like 2,3,7,8-tetrachlorodibenzodioxin (TCDD

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

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

64 mmatory responses by inhibition of canonical AhR signaling.

65 evealed that Langerin-AhR(-/-) but not CD11c-AhR(-/-) mice harbored a decreased number of LC with few

66 In addition, non-CKD AhR(-/-) knockout mice were protected against indoxyl su

67 We used this chemical tool to control AhR activation with spatiotemporal precision within cell

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

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

70 BLG facilitated quercetin-dependent AhR activation and, downstream of AhR, lung Cyp1A1 expre

71 n the gut microbiome and microbially derived AhR ligands protects against inflammation along the gut-

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

73 Despite AhR ChIP-seq enrichment at 2 h, OCM gene expression was

74 gand-free diet supplemented with the dietary AhR ligand indole-3-carbinol (I3C).

75 alteration of fecal microbiota upon dietary AhR ligand deprivation.

76 le indoleamine 2,3-dioxygenase (IDO1) drives AhR activation in other settings, MHV infection induced

77 uced in Th17 cells in the presence of either AhR agonist or CS-enriched medium.

78 n summary, we show that coronaviruses elicit AhR activation by an IDO1-independent pathway, contribut

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

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

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

82 Epidermal LC and CD34LC express AhR and AhRR.

83 ates the activity of a transcription factor (AhR) that regulates immune responses and the biological

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

85 red chemicals did not completely account for AhR and PXR responses.

86 lpha (TNF-alpha), consistent with a role for AhR activation in the host response to MHV infection.

87 highlight a previously unidentified role for AhR in regulating coronavirus replication and the immune

88 identify a previously unappreciated role for AhR signaling in CoV pathogenesis.IMPORTANCE Coronavirus

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

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

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

92 The mechanisms how AhR activates or inhibits cutaneous immune responses rem

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

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

95 Anti-PD-L1 antibody or deficiency in AhR significantly suppresses BaP-induced lung cancer.

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

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

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

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

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

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

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

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

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

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

106 Collectively, the GLK-induced AhR-ROR-gammat (and AhR-phosphorylated ROR-gammat) compl

107 Here, we investigated whether GLK-induced AhR-ROR-gammat complex in T cells is a therapeutic targe

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

109 found that B12/FA deficiency in mice induces AhR transcriptional activity and accumulation of erythro

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

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

112 CD11c-specific knockout ((-/-)) mice lacking AhR, respectively, in LC and Langerin(+) dermal DC and i

113 Langerin-AhR(-/-) mice also exhibited increased blood levels of O

114 py and flow cytometry revealed that Langerin-AhR(-/-) but not CD11c-AhR(-/-) mice harbored a decrease

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

116 Mechanistically, AhR transcriptionally suppresses FoxM1 expression.

117 of transient and stable CRISPR/Cas9-mediated AhR knockdown in GBM cells indicated that loss of AhR en

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

119 observing that kynurenine does not modulate AhR-mediated gene expression and does not affect invasio

120 ive ligand binding affinities for the mutant AhRs.

121 which B12 and FA blunt the effect of natural AhR agonists at baseline to prevent the symptoms that ar

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

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

124 Moreover, in the absence of AhR, we detected an enhanced T helper type-2 (Th2) [incr

125 ed indolo[3,2-b]carbazoles for activation of AhR in cells.

126 Activation of AhR in human organoids recapitulates phenotypes observed

127 urrent study demonstrates that activation of AhR in naive mice triggers robust mobilization of MDSCs

128 -MO and that the 5-HT-mediated activation of AhR is 5-HT(2B) dependent because it is abrogated by the

129 stimulates the transcriptional activation of AhR.

130 Blockade of AhR using a clinically available AhR antagonist greatly

131 chemicals representative of major classes of AhR ligands.

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

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

134 In conclusion, deletion of AhR in langerin-expressing cells diminishes the number a

135 Here, we observed that inducible deletion of AhR in Lgr5(+) stem cells increases the percentage of co

136 Here, we report the development of AhR-activating nanoliposomes (NLPs) to induce antigen-sp

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

138 ion of other genes known to be downstream of AhR in macrophages and dendritic cells and in livers of

139 -dependent AhR activation and, downstream of AhR, lung Cyp1A1 expression.

140 promising combinatorial anticancer effect of AhR and EGFR pathway inhibition.

141 This study examines the effects of AhR activation on hepatic transcriptome and metabolome r

142 We defined effects of AhR deficiency during weight gain or loss in male and fe

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

144 se dependently upregulates the expression of AhR target genes in M-MO and that the 5-HT-mediated acti

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

146 sults, we observed an impaired expression of AhR-regulated genes (eg, CYP1A1) and an upregulation of

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

148 ifferences in the cell-specific functions of AhR and the different activating ligands.

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

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

151 Therapeutically, chemical inhibition of AhR activity sensitizes human BC models to Erlotinib, a

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

153 th progression disease exhibit low levels of AhR in tumor tissues.

154 nse or stable disease express high levels of AhR, whereas 12/16 (75%) patients with progression disea

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

156 nockdown in GBM cells indicated that loss of AhR enhances GBM tumor growth in a mouse xenograft model

157 haceae species, depleted its growth media of AhR ligands.

158 may contribute to differential modulation of AhR functionality.

159 phages, suggesting an alternative pathway of AhR activation.

160 ile acids and by the decreased production of AhR ligands by microbiota that could limit indoleamine 2

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

162 Our data point to the critical role of AhR dietary ligands in shaping the composition and prope

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

164 refore, we sought to investigate the role of AhR in LC and langerin(+) and negative DC in the skin.

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

166 uptake demonstrated higher transcription of AhR target genes and lower transcription of pathways imp

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

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

169 nd confirm that its efficacy is dependent on AhR.

170 Treatment with CXCR2 or AhR antagonist in mice led to marked reduction in TCDD-i

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

172 tively, these results demonstrate persistent AhR activation disrupts hepatic OCM metabolism at the tr

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

174 propose that by spying on bacterial quorum, AhR acts as a major sensor of infection dynamics, capabl

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

176 plant pigment is sensed by the host receptor AhR, and how the physiopathological context determines b

177 The Ah receptor (AhR) is a ligand-dependent transcription factor belongin

178 via binding to the arylhydrocarbon receptor (AhR) and the peroxisome proliferator-activated receptor

179 Aryl hydrocarbon receptor (AhR) activation is reported to alter the hepatic express

180 Aryl hydrocarbon receptor (AhR) activation was evaluated with reporter cells and Cy

181 tion by promoting aryl hydrocarbon receptor (AhR) and hypoxia-inducible factor 1alpha (HIF1alpha) exp

182 The aryl hydrocarbon receptor (AhR) and pregnane X receptor (PXR) transcription factors

183 that targets the aryl hydrocarbon receptor (AhR) and ultimately induces Th17 cell differentiation.

184 (DCs), as well as aryl hydrocarbon receptor (AhR) expression by CD4(+) T cells.

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

186 h17 cells and the Aryl hydrocarbon receptor (AhR) have been implicated, the mechanism by which CS ind

187 level of nuclear aryl hydrocarbon receptor (AhR) in LXA4-treated KSHV-infected cells than in untreat

188 onical pathway of aryl hydrocarbon receptor (AhR) in vitro, thereby inducing the expression of proinf

189 nscription factor aryl hydrocarbon receptor (AhR) is a candidate target for novel immunotherapies.

190 The aryl hydrocarbon receptor (AhR) is a cytoplasmic receptor/transcription factor that

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

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

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

194 we show that the aryl hydrocarbon receptor (AhR) is a target of ezutromid.

195 we show that the aryl hydrocarbon receptor (AhR) is activated in cells infected with a prototypic co

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

197 turally-occurring aryl hydrocarbon receptor (AhR) ligand, allowed its biological and physical propert

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

199 es, especially in aryl hydrocarbon receptor (AhR) ligands, bile acids and plasmalogens.

200 ed a diet free of aryl hydrocarbon receptor (AhR) ligands.

201 ays, for example, aryl hydrocarbon receptor (AhR) or estrogen receptor (ER) activities.

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

203 regulated and the aryl hydrocarbon receptor (AhR) pathway was significantly downregulated in HDM-chal

204 The aryl hydrocarbon receptor (AhR) plays an important role in maintaining cellular hom

205 The aryl hydrocarbon receptor (AhR) represents an environmental sensor regulating immun

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

207 the expression of aryl hydrocarbon receptor (AhR) target genes, and stimulates the transcriptional ac

208 n the host by the aryl hydrocarbon receptor (AhR) that is critically dependent on qualitative and qua

209 as ligands of the aryl hydrocarbon receptor (AhR) to negatively influence health.

210 re ligands of the aryl hydrocarbon receptor (AhR)(6), and AhR-mediated signalling in ILC3 and gammade

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

212 The aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor that sense

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

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

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

216 tor (PXR) and the aryl hydrocarbon receptor (AhR), and itsinteractions with microbial metabolites.

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

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

219 nscription factor aryl hydrocarbon receptor (AhR), which binds TB virulence factors and controls anti

220 ility to activate aryl hydrocarbon receptor (AhR), which is a ligand-dependent transcription factor b

221 nscription factor aryl hydrocarbon receptor (AhR), which is widely expressed in the central nervous s

222 ugh activation of aryl hydrocarbon receptor (AhR)- nuclear factor erythroid 2-related factor 2 (Nrf2)

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

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

225 through inducing aryl hydrocarbon receptor (AhR)-retinoic acid receptor-related orphan nuclear recep

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

227 nscription factor aryl hydrocarbon receptor (AhR).

228 ch is mediated by aryl hydrocarbon receptor (AhR).

229 potent ligand for aryl hydrocarbon receptor (AhR).

230 controlled by the aryl hydrocarbon receptor (AhR).

231 activation of the aryl hydrocarbon receptor (AhR).

232 activation of the aryl hydrocarbon receptor (AhR).

233 al antagonists of aryl hydrocarbon receptor (AhR).

234 tential of LXA4 and its targetable receptor, AhR, in KSHV's pathogenesis.

235 Furthermore, other reported AhR antagonists also upregulate utrophin, showing that t

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

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

238 In the skin, AhR is expressed in several cell types, including kerati

239 Moreover, intestinal-specific AhR knockout increases basal stem cell and crypt injury-

240 Targeting AhR in vivo with a small-molecule inhibitor increases RF

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

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

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

244 Here, we show that AhR is activated in cells infected with mouse hepatitis

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

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

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

248 The AhR also plays important roles in several physiological

249 The AhR and its ligands also inhibit colon carcinogenesis, b

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

251 e re-examined the role of kynurenine and the AhR in GBM, observing that kynurenine does not modulate

252 uction of ROR-gammat phosphorylation and the AhR-ROR-gammat (and AhR-phosphorylated ROR-gammat) compl

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

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

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

256 hought to function through regulation of the AhR and Nrf2 signaling pathways, which have also been li

257 Binding to and activation of the AhR by a variety of chemicals results in the induction o

258 e for understanding ligand modulation of the AhR functionality and for rational drug design.

259 ily focused on investigating the role of the AhR in GBM at the functional molecular and genomic level

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

261 our understanding of the central role of the AhR in skin inflammation and may point toward a potentia

262 lecular docking to the homology model of the AhR LBD that includes the receptor flexibility, we predi

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

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

265 the modulation of the dual functions of the AhR.

266 eae was enriched in the feces of mice on the AhR ligand-free diet but returned to normal levels upon

267 Cultured fecal bacteria from mice on the AhR ligand-free diet, but not the other two diets, were

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

269 As a corollary, we propose the AhR as a potential target for HDT in TB in adjunct to ca

270 nogenesis, but it has been reported that the AhR and its ligand kynurenine enhance glioblastoma (GBM)

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

272 We conclude that the AhR is a tumor suppressor-like gene in GBM; future studi

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

274 These findings indicate that the AhR-FoxM1 axis, at least in part, mediates colonic stem/

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

276 onstrate that in the context of therapy, the AhR binds several TB drugs, including front line drugs r

277 Thus, the AhR markedly impacts TB outcome by affecting both host d

278 We postulate a hypothesis where the AhR (aryl hydrocarbon receptor) mediates aberrant cell g

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

280 dies are required to investigate whether the AhR could be a potential drug target for treating patien

281 NLPs loaded with the AhR agonist ITE and a T cell epitope from myelin oligode

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

283 y, we predicted specific residues within the AhR binding cavity that play a critical role in binding

284 e interactions of various ligands within the AhR ligand binding domain (LBD) may contribute to differ

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

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

287 Thus, AhR represents an attractive target to inhibit redox hom

288 QS molecules bind to AhR and distinctly modulate its activity.

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

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

291 ay point toward a potential role for topical AhR agonists in supportive cancer care.

292 Mechanistically, ROS triggers AhR nuclear accumulation and activation to promote the t

293 ich diet or by 5/6 nephrectomy; we also used AhR(-/-) knockout mice overloaded with indoxyl sulfate i

294 We show that TGF-beta, via AhR induction, and PI3K signaling promotes IL-22 product

295 e show that indoxyl sulfate induces OAT1 via AhR and EGFR signaling, controlled by miR-223.

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

297 h of sorted stem and progenitor cells, while AhR activation has the opposite effect.

298 line to prevent the symptoms that arise with AhR overactivation.

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

300 Surface waters with AhR and PXR effects were associated with low intensity,