ライフサイエンスコーパス: AHR

1 AHR activation induces cytochrome P4501 (CYP1) enzymes,

2 AHR expression and responsiveness along with H3K4me2 wer

3 AHR is common in patients with mild-to-moderate COPD, af

4 AHR is highly expressed in hematopoietic stem and progen

5 AHR knockdown or inhibition significantly reduces TDO2 e

6 AHR may represent a spectrum of the asthma-COPD overlap

7 AHR-New was selected as the proposed ICON-S stage classi

8 with cell-mediated immunity; 2p22.3; 7p21.1 AHR, the dioxin receptor involved in anti-apoptotic path

9 or NK cell development, GATA3, TCF7 (TCF-1), AHR, SOX4, RUNX2, and ZEB1 transcript levels are higher

10 e distal colon with mutant KRAS in codon 12 (AHR, 1.76; 95% CI, 1.30-2.38; P < .001) and codon 13 (AH

11 ; 95% CI, 1.30-2.38; P < .001) and codon 13 (AHR, 1.76; 95% CI, 1.08-2.86; P = .02).

12 elvic inflammatory disease by a further 20% (AHR 1.20, 95% CI 1.11-1.31).

13 enged mice, anti-IgE mAb treatment abolished AHR 24 hour and 48 hour after the last challenge and sig

14 tary tryptophan by the gut flora to activate AHR signaling in astrocytes and suppress CNS inflammatio

15 n addition, we reveal that agonist-activated AHR impairs PPARalpha-, ChREBP-, and CREBH-mediated prom

16 dditionally, binding of the ligand-activated AHR to the putative dioxin response elements in the EBF1

17 s Arid1a to the Ahr promoter thus activating AHR expression.

18 eg, IVIg failed to confer protection against AHR and airway inflammation.

19 found that TSG-6 deficiency protects against AHR after ozone (in vivo) or sHA (in vitro and in vivo)

20 Activation of pDCs alleviates AHR and airway inflammation by suppressing ILC2 function

21 provides evidence that kynurenine acts as an AHR pro-ligand, which requires novel chemical conversion

22 B6 mice fed an AHR ligand-deficient, semipurified diet have significant

23 Addition of an AHR antagonist reversed 2,3,7,8-tetrachlorodibenzo-p-dio

24 abolizing tryptophan or by treatment with an AHR agonist.

25 osinophils and inflammation, IL-5, IL-13 and AHR.

26 udies highlight the potential of the AHR and AHR ligands as future therapeutic options for eye diseas

27 The AHR and AHR ligands block profibrotic Wnt signaling by inhibitin

28 C57BL/6 (B6), AHR, and AHR mice were placed on either grain-based or semipurifi

29 e correlation between urea-1-carboxylate and AHR was observed in plasma metabolites, while ornithine

30 duced the production of type 2 cytokines and AHR.

31 was associated with airway eosinophilia and AHR to mannitol but not airway neutrophilia.

32 ffectively prevented airway inflammation and AHR in an Ag-specific manner.

33 effectively inhibits airway inflammation and AHR in experimental COPD models, prospectively through i

34 ration of steroid-resistant inflammation and AHR secondary to allergen- and pathogen-induced exacerba

35 predominantly eosinophilic inflammation and AHR.

36 extensive heterodimerization interfaces and AHR interdomain interactions.

37 Together, IS and AHR have potential as uremia-specific biomarkers and tar

38 mined the relationship between IS levels and AHR-inducing activity in sera of patients with ESRD.

39 AChR agonist reduces cytokine production and AHR in a humanized ILC2 mouse model.

40 t LPS/IFN-gamma-induced IL-27 production and AHR in mice.

41 k LPS/IFN-gamma-induced IL-27 production and AHR via its antioxidative property.

42 itative PCR), inflammatory cell profile, and AHR (flexiVent) were assessed in the mice.

43 sed to ozone or short-fragment HA (sHA), and AHR was assayed via flexiVent.

44 fied compound in both chemical structure and AHR pharmacology.

45 -3-carbinol (I3C), a dietary supplement, and AHR precursor ligand in a murine model of CDI.

46 ncovered AHR as an antithrombotic target and AHR antagonists as a novel class of antithrombotics.

47 oalveolar lavage fluid and lung tissues, and AHR in mice.

48 nscriptionally active heterodimer with ARNT (AHR nuclear translocator), which recognizes the dioxin r

49 lex with the DRE, in which ARNT curls around AHR into a highly intertwined asymmetric architecture, w

50 We identify TFs, such as AHR, which become inactivated in the earliest stages of

51 ination with IL-17A significantly attenuated AHR and mucus metaplasia.

52 C57BL/6 (B6), AHR, and AHR mice were placed on either grain-based or s

53 rected migration in vivo and aggravated both AHR and eosinophil influx into the airways in a CB2 -spe

54 ortant role in murine asthma, mediating both AHR and mucus secretion after HDM exposure.

55 Lastly, we demonstrated that both AHR and NR2E3 are significantly associated with good cli

56 ings indicate I3C may be acting through both AHR-dependent and -independent mechanisms in this model.

57 ents whose tumors harbored mutant BRAFV600E (AHR, 2.45; 95% CI, 1.85-3.25; P < .001) or mutant KRAS (

58 esting transcriptional regulation of EBF1 by AHR.

59 interferon (IFN)-beta are partly mediated by AHR.

60 MMR tumors of the proximal vs distal colon (AHR, 0.57; 95% CI, 0.40-0.83; P = .003), and worse SAR w

61 allergen-exposed mice, loss of Plgf dampened AHR, reduced inflammation and eosinophilia, and decrease

62 h an increased risk of cardiovascular death (AHR, 3.09; 95% CI, 2.46-3.89; P < .001), myocardial infa

63 ransferred with Th2/Th17 cells had decreased AHR compared with controls.

64 For the primary analysis, we defined AHR by a methacholine provocation concentration of 4 mg/

65 fector function and represses ILC2-dependent AHR, while decreasing expression of ILC2 key transcripti

66 hydrocarbon receptor (AHR) and diet-derived AHR ligands in mucosal immunity.

67 ) malignant cells produce tryptophan-derived AHR ligand(s) through the kynurenine pathway; 2) these m

68 hematopoietic system were mediated by direct AHR activation in the fetus.

69 e never-tested (pelvic inflammatory disease, AHR 0.33 [0.31-0.35]; ectopic pregnancy, AHR 0.42 [0.39-

70 hese metabolites have the potential to drive AHR-dependent breast cancer migration; 3) the AHR contro

71 These data suggest that IL-13 drives AHR and mucus metaplasia in a STAT6-dependent manner, wi

72 t the interdomain interactions caused either AHR constitutive nuclear localization or failure to tran

73 nt TDO2 expression contributes to endogenous AHR ligand production.

74 he importance of determining what endogenous AHR ligands are produced, how their production is regula

75 sed amplification loop; and 4) environmental AHR ligands mimic the effects of endogenous ligands.

76 al response, airway and tissue eosinophilia, AHR, and TH2 and TH17 pulmonary profiles.

77 our findings indicate that PlGF exacerbates AHR and uniquely links the leukotriene and Th2 pathways

78 The deleterious effects of excessive AHR ligand degradation on intestinal immune functions co

79 and challenged with CE for 12 weeks exhibit AHR, increased numbers of eosinophils in bronchoalveolar

80 4) and > 5 mitoses per 50 high-power fields (AHR, 2.5; 95% CI, 1.1 to 6.0; P = .03), whereas there wa

81 Finally, AHR activation correlated with mo-DC infiltration in lep

82 ociated with preterm birth during the first (AHR = 1.84, 95% CI: 1.14, 2.98), second (AHR = 1.89, 95%

83 ed tissue and context-specific functions for AHR in both homeostasis and in during an immune response

84 TSG-6 is necessary for AHR in allergic asthma, because it facilitates the devel

85 In conclusion, TSG-6 is necessary for AHR in response to ozone or sHA, in part because it faci

86 Downstream molecular targets responsible for AHR-dependent adverse effects remain largely unknown; ho

87 HR, with identical structural signatures for AHR induction before and after activation.

88 Furthermore, AHR antagonists inhibited TF in a manner dependent on ci

89 Approximately 24% of LHS participants had AHR.

90 2.67; P < .001), and hospitalization for HF (AHR, 3.85; 95% CI, 2.82-5.27; P < .001).

91 2.53; P < .001), and hospitalization for HF (AHR, 3.92; 95% CI, 3.11-4.92; P < .001).

92 ortality, the mechanisms underlying the high AHR prevalence in a hemoglobinopathy remain unknown.

93 with pregnane X (PXR) and aryl hydrocarbon (AHR) receptors, it is referred to as "xenobiotic recepto

94 t is associated with airway hyperreactivity (AHR) and driven by Th2 cytokine secretion.

95 on and ILC2-mediated airway hyperreactivity (AHR) and lung inflammation.

96 underlies prolonged airway hyperreactivity (AHR) in mice.

97 Airway hyperresponsiveness (AHR) affects 55%-77% of children with sickle cell diseas

98 Airway hyperresponsiveness (AHR) and bronchial inflammation were analyzed after intr

99 protects against airway hyperresponsiveness (AHR) and inflammation in mouse models of allergic airway

100 rial LPS-induced airway hyperresponsiveness (AHR) and lung inflammation, and bleomycin-induced lung f

101 cantly increased airway hyperresponsiveness (AHR) and macrophage and neutrophil lung infiltration.

102 proliferation in airway hyperresponsiveness (AHR) associated with asthma are still largely unknown.

103 inflammation and airway hyperresponsiveness (AHR) following allergen challenge, whereas mice sensitiz

104 inflammation and airway hyperresponsiveness (AHR) in acute murine models.

105 n a reduction of airway hyperresponsiveness (AHR) when using triple therapy.

106 extract-induced airway hyperresponsiveness (AHR), airway inflammation, immunoglobulin production, TH

107 allergen-induced airway hyperresponsiveness (AHR), airway resistance, and compliance in response to m

108 low obstruction, airway hyperresponsiveness (AHR), and airway inflammation.

109 onist attenuates airway hyperresponsiveness (AHR), eosinophilic inflammation, and mucus-production re

110 th sGARP reduced airway hyperresponsiveness (AHR), influx of neutrophils and macrophages into the bro

111 17A in mediating airway hyperresponsiveness (AHR), lung inflammation, and mucus metaplasia in a dual

112 ted reduction in airway hyperresponsiveness (AHR), OVA allergen-challenged Ormdl3(Delta2-3/Delta2-3)/

113 nase (5-LO)] and airway-hyperresponsiveness (AHR) (5-LO).

114 cretion, remodeling and hyperresponsiveness (AHR).

115 airway inflammation and hyperresponsiveness (AHR).

116 -oxidative capacity, on hyperresponsiveness (AHR) and inflammation in experimental models of COPD.

117 ering OVA-induced airway hyperresponsivness (AHR), which was unattainable by eight times of SCIT over

118 Among these regulatory factors, we identify AHR, the aryl hydrocarbon-receptor which controls a heal

119 Moreover, Arid1a deletion impedes AHR expression and impairs the maintenance of NKp46(+) I

120 showed a significant spontaneous increase in AHR and a significant spontaneous increase in airway rem

121 2-3)/CC10 mice had a significant increase in AHR compared with wild-type mice.

122 action and to investigate its involvement in AHR associated with allergic asthma.

123 decipher in vivo the implication of Rac1 in AHR.

124 AHR null mice had less of an impact than in AHR heterozygous littermates, although some protection w

125 all features of allergic disease, including AHR and eosinophil infiltration, in uninfected OVA-sensi

126 Airway obstruction, including AHR and airway resistance, was diminished in allergen-ch

127 of HDM-exposed mothers demonstrate increased AHR, airway inflammation, TH2 cytokine production, and i

128 In an SCD mouse model, we observed increased AHR and higher leukotriene levels that were abrogated by

129 helium is sufficient to rescue IL-13-induced AHR, inflammation, and mucus production, and transgenic

130 CC10 mice exhibit increased allergen-induced AHR independent of inflammation and associated with incr

131 tory cytokines and improves allergen-induced AHR, airway resistance, and compliance.

132 AR2 signaling plays a key role in CE-induced AHR and airway inflammation/remodeling in long term mode

133 hers also demonstrated increased HDM-induced AHR, suggesting that transfer of maternal immunoglobulin

134 ere sufficient for inhibition of OVA-induced AHR in an Ag-driven murine model of AAD.

135 for the development of HA- and ozone-induced AHR.

136 2.46-3.89; P < .001), myocardial infarction (AHR, 1.95; 95% CI, 1.51-2.53; P < .001), and hospitaliza

137 2.35-4.02; P < .001), myocardial infarction (AHR, 2.13; 95% CI, 1.69-2.67; P < .001), and hospitaliza

138 R 0.42 [0.39-0.44]; tubal factor infertility AHR 0.29 [0.25-0.33]).

139 1.31 [1.25-1.38]; tubal factor infertility, AHR 1.37 [1.24-1.52]) and 60% lower in women who were ne

140 Airway inflammation, AHR, resistance, and compliance were assessed in Il15 ge

141 tion of PAR2 prevents allergic inflammation, AHR and airway remodeling in chronic allergic airway inf

142 an is metabolized by the gut microbiota into AHR agonists that have an effect on astrocytes to limit

143 Using ITPR3, AHR and NMU as examples, we explored and validated how t

144 95% CI, 1.85-3.25; P < .001) or mutant KRAS (AHR, 1.21; 95% CI, 1.00-1.47; P = .052) had worse SAR co

145 found that an orphan nuclear NR2E3 maintains AHR expression, and forms an active transcriptional comp

146 which AHR2 (functional ortholog of mammalian AHR) activation leads to reduced sox9b expression levels

147 mined the crystal structure of the mammalian AHR-ARNT heterodimer in complex with the DRE, in which A

148 t of negative microscopic resection margins (AHR, 0.9; 95% CI, 0.4 to 2.2; P = 0.86).

149 re, the control mice responded with a marked AHR and airway inflammation.

150 ERK, or PI3K/Akt blocked sHA/TSG-6-mediated AHR.

151 eek model of cockroach extract (CE)-mediated AHR, airway inflammation and remodeling in BALB/c mice.

152 l-like receptor 7/8 suppresses ILC2-mediated AHR and airway inflammation and that depletion of pDCs r

153 Therefore, WASH-mediated AHR expression has a critical function in the maintenanc

154 ted factor that is elevated in SCD, mediates AHR.

155 importance of feedback control in modulating AHR pathway activation.

156 in vitro and in vivo were examined and mouse AHR was assessed.

157 a1 in mice depletes the reservoir of natural AHR ligands, generating a quasi AHR-deficient state.

158 3 (near CD83) and several SNPs at 7p21 (near AHR), 15q24 (near CYP1A2) and 19q13.2 (near CYP2A6) met

159 hand, the Igf1r-deficient mice exhibited no AHR, and a selective decrease in blood and BALF eosinoph

160 r results reveal a novel link between NR2E3, AHR, and liver cancer via LSD1-mediated H3K4me2 histone

161 1 Furthermore, in vivo agonist activation of AHR reduces hepatic Fgf21 expression during a fast.

162 s determined by three factors: the amount of AHR in any given cell, the abundance and potency of AHR

163 vented mucus accumulation and development of AHR in mice.

164 contraction of aSMCs, and the development of AHR.

165 The addition of I3C to the diet of AHR null mice had less of an impact than in AHR heterozy

166 feedback role that curtails the duration of AHR signalling, but it remains unclear whether they also

167 ic segregation, we examined the influence of AHR expression upon intestinal microbe composition/funct

168 d progenitor cells (HSPCs) and inhibition of AHR results in a marked expansion of human umbilical cor

169 counter-balanced by increasing the intake of AHR ligands in the diet.

170 We investigated the involvement of AHR, a ligand-activated transcriptional regulator, in co

171 dividuals with MS, the circulating levels of AHR agonists were decreased.

172 and their metastases, express high levels of AHR and tryptophan-2,3-dioxygenase (TDO); representative

173 estinal epithelial cells resulted in loss of AHR-dependent type 3 innate lymphoid cells and T helper

174 ently, environmental/genetic manipulation of AHR activity likely influences host-microbe homeostasis.

175 As the known number of AHR-mediated processes grows, so too does the importance

176 on the hydrophobic ligand-binding pocket of AHR, with identical structural signatures for AHR induct

177 any given cell, the abundance and potency of AHR ligands within certain tissues, and the tissue micro

178 Reduced production of AHR ligands is also observed in the microbiota from indi

179 (ChRM)-3 blocker reversed the progression of AHR in the neonatal exposure model, whereas beta2-adreno

180 We sought to determine the relationship of AHR with FEV1 decline, respiratory mortality, and system

181 promoter region, resulting in repression of AHR expression.

182 Here, we explore the role of AHR in hepatic Fgf21 expression through the use of a con

183 However, the role of AHR in human B cell development has not been investigate

184 arly B and pro-B cells, suggesting a role of AHR in regulating B lymphopoiesis.

185 We examined the role of AHR using both an Ahr-deletion mouse model (Ahr) and tre

186 tructural hierarchy for complex scenarios of AHR activation induced by its diverse ligands.

187 ific genetic approaches towards the study of AHR function.

188 cells serve as gatekeepers for the supply of AHR ligands to the host and emphasize the importance of

189 ut life suggests that the cellular target of AHR activation is a fetal hematopoietic progenitor or st

190 oxicity that correlated with upregulation of AHR, MED1, and CYP1A2 expression.

191 This study supports the use of AHR agonists such as I3C as a chemopreventive therapy fo

192 formation, and this ability is dependent on AHR expression.

193 Pregnant C57BL/6 or AHR+/- mice were exposed to the AHR agonist, 2,3,7,8-tet

194 chrome P4501 (CYP1) enzymes, which oxygenate AHR ligands, leading to their metabolic clearance and de

195 uniquely in early life to induce persistent AHR after allergen exposure.

196 is necessary for the induction of persistent AHR after neonatal exposure during rescue assays in mice

197 se, AHR 0.33 [0.31-0.35]; ectopic pregnancy, AHR 0.42 [0.39-0.44]; tubal factor infertility AHR 0.29

198 1.50 [95% CI 1.43-1.57]; ectopic pregnancy, AHR 1.31 [1.25-1.38]; tubal factor infertility, AHR 1.37

199 bition by nebulization of NSC23766 prevented AHR in murine models of allergic asthma.

200 imated clinical effectiveness of primaquine (AHR 0.91, 95% CI 0.85-0.97, p = 0.003).

201 kg) or high (>/=5 mg/kg) dose of primaquine (AHR = 0.90 [95% CI 0.86-0.95, p < 0.001]).

202 Humanized mice displayed a more pronounced AHR and bronchial inflammation when challenged with alle

203 r of natural AHR ligands, generating a quasi AHR-deficient state.

204 but significantly higher ART attrition rate (AHR: 1.17, 95% CI: 1.03-1.33).

205 ke of plant nitrites (adjusted hazard ratio (AHR) = 0.72, 95% confidence interval (CI): 0.53, 0.97).

206 [95% CI 23.4-24.9%]); Adjusted Hazard Ratio (AHR) = 2.23 (95% CI 2.15-2.31), p < 0.001.

207 inflammatory disease, adjusted hazard ratio [AHR] 1.50 [95% CI 1.43-1.57]; ectopic pregnancy, AHR 1.3

208 ificantly better SAR (adjusted hazard ratio [AHR], 0.70; 95% CI, 0.52-0.96; P = .03).

209 h metastatic disease (adjusted hazard ratio [AHR], 2.3; 95% CI, 1.0 to 5.1; P = .04) and > 5 mitoses

210 cardiovascular death (adjusted hazard ratio [AHR], 3.07; 95% CI, 2.35-4.02; P < .001), myocardial inf

211 es eosinophilia and airway hyper-reactivity (AHR), which are cardinal features of asthma.

212 ne a role for the aryl hydrocarbon receptor (AHR) and diet-derived AHR ligands in mucosal immunity.

213 the elevation of aryl hydrocarbon receptor (AHR) and mediator 1 (MED1), two transactivators of Cyp1a

214 nscription factor aryl hydrocarbon receptor (AHR) and the suppressor of cytokine signaling 2 (SOCS2).

215 he IL-1 inhibitor aryl hydrocarbon receptor (AHR) at baseline and accumulated higher levels of intrac

216 The aryl hydrocarbon receptor (AHR) belongs to the PAS (PER-ARNT-SIM) family transcript

217 activation of the aryl hydrocarbon receptor (AHR) by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) preve

218 Aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that med

219 The aryl hydrocarbon receptor (AHR) is an important regulator of the development and fu

220 The aryl hydrocarbon receptor (AHR) is emerging as a pleiotropic factor, modulating pat

221 that activate the aryl hydrocarbon receptor (AHR) lead to suppression of immune system function throu

222 lites that act as aryl hydrocarbon receptor (AHR) ligands.

223 The aryl hydrocarbon receptor (AHR) plays an important physiological role in hematopoie

224 ligand-activated aryl hydrocarbon receptor (AHR) plays an important role in numerous biologic proces

225 The aryl hydrocarbon receptor (AHR) plays crucial roles in inflammation, metabolic diso

226 Activation of the aryl hydrocarbon receptor (AHR) promoted mo-DC differentiation through the inductio

227 The aryl hydrocarbon receptor (AHR) recognizes xenobiotics as well as natural compounds

228 is influenced by aryl hydrocarbon receptor (AHR) signaling pathways.

229 s depend upon the aryl hydrocarbon receptor (AHR), a conserved detector of xenobiotic small molecules

230 ine activates the aryl hydrocarbon receptor (AHR), a PER, ARNT, SIM (PAS) family transcription factor

231 of the mammalian aryl hydrocarbon receptor (AHR), and UPEC infection of Ahr(-/-)mice recapitulated t

232 an agonist of the aryl hydrocarbon receptor (AHR), we first examined the relationship between IS leve

233 activation of the aryl hydrocarbon receptor (AHR).

234 t remains unclear whether they also regulate AHR ligand availability in vivo.

235 nderstanding of the mechanisms that regulate AHR transcription and function.

236 n in asthma is previously unknown, regulates AHR and airway remodeling without airway inflammation th

237 However, the molecular mechanisms regulating AHR expression remain unknown.

238 Airway hyper-responsiveness (AHR) measurements and differential cell counts were perf

239 Airway hyper-responsiveness (AHR) using a methacholine test, airway inflammation in b

240 as a measure of airway hyper-responsiveness (AHR), and lung histology and viral replication were asse

241 bulin (Ig)E and airway hyper-responsiveness (AHR).

242 ction (LF), and airway hyper-responsiveness (AHR).

243 flammation, and airway hyper-responsiveness (AHR).

244 SP2509, an LSD1 inhibitor, fully restored AHR expression and H3K4me2 levels in Rd7 mice.

245 st (AHR = 1.84, 95% CI: 1.14, 2.98), second (AHR = 1.89, 95% CI: 1.17, 3.07), and third (AHR = 2.00,

246 g RNA (slincR) that is upregulated by strong AHR ligands and is located adjacent to the sox9b gene.

247 duced exacerbation only partially suppressed AHR and failed to dampen macrophage and neutrophil infil

248 he use of a conditional, hepatocyte-targeted AHR knock-out mouse model (Cre(Alb)Ahr(Fx/Fx)).

249 Antagonists directly targeting AHR enhanced TF ubiquitination and degradation and suppr

250 Collectively, these results demonstrate that AHR regulates early human hematolymphoid cell developmen

251 Supporting the demonstration that AHR down-regulation skews monocytes toward macrophage di

252 Using this model, we found that AHR activation by the high-affinity ligand 2,3,7,8-tetra

253 We found that AHR ligands prevent TGF-beta-dependent myofibroblast for

254 We found that AHR plays a protective role in colitis-associated colore

255 Our findings indicate that AHR activation by TCDD in the fetus during pregnancy lea

256 Several studies indicate that AHR is also involved in energy homeostasis.

257 distinct transcription factors and show that AHR acts as a molecular switch for monocyte fate specifi

258 Together, our data show that AHR contributes to hepatic energy homeostasis, partly th

259 The AHR and AHR ligands block profibrotic Wnt signaling by i

260 The AHR forms a transcriptionally active heterodimer with AR

261 The AHR is known to regulate immune surveillance within the

262 The AHR response to sHA was evaluated in the isolated trache

263 HR-dependent breast cancer migration; 3) the AHR controls expression of a rate-limiting kynurenine pa

264 d concentrations to chronically activate the AHR.

265 Ab administration in WT animals blunted the AHR.

266 t transcriptional alterations of EBF1 by the AHR are involved in the underlying mechanism.

267 ther, this study demonstrates a role for the AHR in regulating human B cell development, and it sugge

268 novel studies highlight the potential of the AHR and AHR ligands as future therapeutic options for ey

269 in defined conditions in the presence of the AHR antagonist StemReginin-1 (SR-1) or the AHR agonist 2

270 er with the global higher flexibility of the AHR PAS-A and its loosely packed structural elements, su

271 tent concentrations of three agonists of the AHR, 2,3,7,8-TCDD, PCB 77, and benzo[a]pyrene, in livers

272 e pathways associated with activation of the AHR.

273 e AHR antagonist StemReginin-1 (SR-1) or the AHR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

274 d Foxp4-mutant airway epithelium rescued the AHR phenotype.

275 Increasing evidence shows that the AHR plays physiological roles in regulating development,

276 Using EMSA, we demonstrate that the AHR-ARNT heterodimer binds to a specific DRE that overla

277 uction of kynurenines, which act through the AHR to impair neutrophil chemotaxis.

278 t C57BL/6 or AHR+/- mice were exposed to the AHR agonist, 2,3,7,8-tetra-chlorodibenzo-p-dioxin (TCDD)

279 mprovement in asthma features related to the AHR and airway inflammation.

280 3 lysine 4 di-methylation (H3K4me2), to the AHR gene promoter region, resulting in repression of AHR

281 ion mouse model (Ahr) and treatment with the AHR pro-agonist indole-3-carbinol (I3C).

282 (AHR = 1.89, 95% CI: 1.17, 3.07), and third (AHR = 2.00, 95% CI: 1.22, 3.29) trimesters.

283 rated that IS regulates TF stability through AHR signaling and uncovered AHR as an antithrombotic tar

284 IL-17A independently contributes to AHR, but it only partially mediates inflammation and muc

285 tability through AHR signaling and uncovered AHR as an antithrombotic target and AHR antagonists as a

286 vels correlated significantly with both vSMC AHR activity and TF activity.

287 ues, and the tissue microenvironment wherein AHR(+) cells reside.

288 We also evaluated whether AHR antagonism could promote innate lymphoid cell differ

289 It is unknown whether AHR also contributes earlier in human hematopoietic deve

290 I propose a conceptual framework in which AHR function is determined by three factors: the amount

291 time, a positive amplification loop in which AHR-dependent TDO2 expression contributes to endogenous

292 e immune cells through roles associated with AHR's ability to respond to cellular and dietary ligands

293 -5 and IL-13 showed strong correlations with AHR and monocyte chemoattractant protein (MCP)-1 with as

294 -treatment of primary human hepatocytes with AHR agonist diminishes PPARalpha-, glucose-, and ER stre

295 hESC-RUNX1c-tdTomato reporter cell line with AHR deletion, we further demonstrate a marked enhancemen

296 red with patients without AHR, patients with AHR had a 2-fold increased risk of respiratory mortality

297 Patients with AHR had generally reduced burden of systemic inflammator

298 ven Fgf21 expression, and pre-treatment with AHR antagonist blocks this effect.

299 Compared with patients without AHR, patients with AHR had a 2-fold increased risk of re

300 flammatory biomarkers than did those without AHR.