ライフサイエンスコーパス: AHR

1 AHR also drives the expression of KLF4 and suppresses NF

2 AHR and its transcriptional binding partner, ARNT were d

3 AHR bound and activated the gene promoter of serine palm

4 AHR expression and responsiveness along with H3K4me2 wer

5 AHR inhibition suppressed the replication of multiple ZI

6 AHR is a ligand-activated transcription factor that has

7 AHR knockdown in glioblastoma cells also reduced the exp

8 AHR knockout HeLa cells exhibited significantly reduced

9 AHR promotes CCR2 expression, driving TAM recruitment in

10 AHR-activating potencies of Turkish, filter, and instant

11 tients had lower mortality (12.7% vs. 14.3%, AHR: 0.86; 95% CI: 0.79 to 0.93), a lower composite outc

12 eat revascularization rate (11.7% vs. 14.6%, AHR: 0.80; 95% CI: 0.74 to 0.87).

13 a lower composite outcome (20.2% vs. 22.8%, AHR: 0.88; 95% CI: 0.83 to 0.93), and a lower repeat rev

14 (AHR = 6.2, 95% CI 4.6-8.5; p < 0.001), AA (AHR = 2.3, 95% CI 1.4-3.7; p = 0.001), or AM (AHR = 1.4,

15 mption were replicated (in/near GCKR, ABCG2, AHR, POR and CYP1A1/2).

16 1 expression, telltale signs of an activated AHR-TF/PAI-1 axis.

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

18 kynurenine (Kyn) production, which activates AHR, limiting the production of type I interferons (IFN-

19 kemic stem cells (LSC), therefore activating AHR signaling is a potential therapeutic option to targe

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

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

22 in nine genetic loci (MCL1-ENSA, GCKR, AGR3-AHR, ADH1B, ALDH1B1, ALDH1A1, ALDH2, CYP1A2-CSK and ADOR

23 e of recurrence assessed at day 42 after AL (AHR = 0.20, 95% CI 0.10-0.41, p < 0.001) and at day 63 a

24 -19.5; p = 0.002); patients treated with AL (AHR = 6.2, 95% CI 4.6-8.5; p < 0.001), AA (AHR = 2.3, 95

25 no work to date has examined whether altered AHR signaling plays a pathologic role in human AML or wh

26 HR = 2.3, 95% CI 1.4-3.7; p = 0.001), or AM (AHR = 1.4, 95% CI 1.0-1.9; p = 0.028) compared with DP;

27 PD-1 agonist and show that it can ameliorate AHR and suppresses lung inflammation in a humanized mous

28 -1) levels in venous endothelial cells in an AHR-dependent manner.

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

30 T cells that promote airway inflammation and AHR after antigen challenge, suggesting that IL-22 plays

31 ase in allergen-induced Th2 inflammation and AHR in a mouse model of severe steroid resistant asthma,

32 DGK diminished both airway inflammation and AHR in mice and also reduced bronchoconstriction of huma

33 We measured airway inflammation and AHR in wild-type, RAGE(-/-) , TLR4(-/-) and TLR4(-/-) RA

34 neutrophil-dominated airway inflammation and AHR in WT mice, suggesting that loss of IL-22 synergy wi

35 neutrophil-dominated airway inflammation and AHR on intranasal OVA challenge.

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

37 ultaneously reducing airway inflammation and AHR though independent mechanisms.

38 d the development of airway inflammation and AHR, even if treatment occurred only during the challeng

39 d Alternaria-induced airway inflammation and AHR.

40 d the development of airway inflammation and AHR.

41 predominantly eosinophilic inflammation and AHR.

42 asthma and reveal that the inflammatory and AHR components of asthma are not as interdependent as ge

43 tors correlates with airway neutrophilia and AHR in COPD patients.

44 may protect against airway neutrophilia and AHR in COPD.

45 rotected against CS-induced neutrophilia and AHR.

46 cted against CS-induced mediator release and AHR.

47 5% CI: 1.36 to 3.76; p = 0.002 for TRVol and AHR: 2.60; 95% CI: 1.45 to 4.66; p = 0.001 for TRF).

48 i for bitter non-alcoholic beverages (ANXA9, AHR, POR, CYP1A1/2 and CSDC2); (iii) 10 loci for coffee;

49 TP53, ATM, ARID1A, AHR, and SMARCB1 mutations were more frequent in PD.

50 The RGS4 antagonist CCG203769 attenuated AHR induced by allergen or aspirin challenge of wild-typ

51 uMT mice before HDM-sensitization attenuated AHR and lung remodeling.

52 ent when compared to the ART containing AZT (AHR = 0.91, 95% CI: 0.69-1.20).

53 d4T (AHR = 0.72, 95% CI: 0.60-0.86) or AZT (AHR = 0.67, 95% CI: 0.58-0.77).

54 tivity as a critical regulator of beneficial AHR signaling in the context of skin inflammation.

55 skin immunopathology by restoring beneficial AHR signaling.

56 Blocking the interaction between AHR and kynurenine with CH223191 reduced the proliferati

57 reduced levels of cell-surface Gb3, and both AHR knockout HeLa cells and tissues from Ahr knockout mi

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

59 , FICZ-induced MMP1 expression required both AHR and ARNT, demonstrating that the AHR-ARNT transcript

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

61 esting transcriptional regulation of EBF1 by AHR.

62 ciated macrophages, which can be reversed by AHR inhibition.

63 er risk of being hospitalized for any cause (AHR = 1.8 [95% CI: 1.0-3.0], P = .037) and diarrheal (AH

64 After incubation with Caco-2 cells, AHR activity of different coffees was between 35 and 64%

65 Coffee samples showed considerable AHR-activating potencies in DR CALUX(R) bioassay (up to

66 d to those receiving the ART containing d4T (AHR = 0.72, 95% CI: 0.60-0.86) or AZT (AHR = 0.67, 95% C

67 ar their initial parasitaemia within 2 days (AHR = 1.8, 95% CI 1.4-2.3; p < 0.001).

68 neutrophil airway infiltration and decreased AHR after intranasal OVA challenge.

69 zeta in airway smooth muscle cells decreased AHR but not airway inflammation.

70 AHR inhibition with a nanoparticle-delivered AHR antagonist or an inhibitor developed for human use l

71 tion, both wild-type and muMT mice developed AHR, but the AHR was significantly stronger in muMT mice

72 Thus, developmental AHR activation shapes T cell responsive capacity later i

73 [95% CI: 1.0-3.0], P = .037) and diarrheal (AHR = 3.5 [95% CI: 1.3-9.6], P = .016).

74 .10-0.41, p < 0.001) and at day 63 after DP (AHR = 0.08, 95% CI 0.01-0.70, p = 0.0233).

75 TLR9 activation alleviates ILC2-driven AHR and airway inflammation through direct suppression o

76 itution of wild-type ILC2 rescued RSV-driven AHR in IL-13-deficient mice.

77 -derived IL-13 was sufficient for RSV-driven AHR, since reconstitution of wild-type ILC2 rescued RSV-

78 Thus environmental AHR agonists, and potentially also endogenous, nutrition

79 As the blockade of PD-1 exacerbates AHR, we also develop a human PD-1 agonist and show that

80 The transcription factor AHR (aryl hydrocarbon receptor) drives the expression of

81 Activation of the transcription factor, AHR, in normal human epidermal keratinocytes increased A

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

83 Finally, AHR drives the expression of the ectonucleotidase CD39 i

84 Finally, AHR inhibition with a nanoparticle-delivered AHR antagon

85 then challenged with IL-33 and assessed for AHR and lung inflammation.

86 sthma who were extensively characterized for AHR.

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

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

89 Our findings identify a role for AHR in limiting tissue damage during malaria.

90 onsistent with a tumour suppressive role for AHR.

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

92 prescribed pharmaceuticals, may protect from AHR-mediated steatosis, but alter glycogen metabolism an

93 TCDD (S + T) co-treatment increased hepatic AHR-battery gene expression and liver injury in male, bu

94 CD39 was highest in grade 4 glioma, and high AHR expression was associated with poor prognosis.

95 All obese mice showed higher AHR at 30 mg/ml of methacholine compared to CD and food

96 Altogether, this work highlights AHR signaling suppression as a key LSC-regulating contro

97 , this has far-reaching implications for how AHR signaling, particularly during development, durably

98 G A in IL-33-induced airway hyperreactivity (AHR) and airway inflammation.

99 der characterized by airway hyperreactivity (AHR) and driven by T(H)2 cytokine production.

100 egulatory B cells on airway hyperreactivity (AHR) and remodeling in asthma is poorly understood.

101 underlies prolonged airway hyperreactivity (AHR) in mice.

102 way inflammation and airway hyperreactivity (AHR), a cardinal feature of asthma.

103 sible for triggering airway hyperreactivity (AHR), inflammation and eosinophilia remained to be clari

104 nst allergen-induced airway hyperreactivity (AHR).

105 ease associated with airway hyperreactivity (AHR).

106 ted in increased airway hyperresponsiveness (AHR) and accumulation of pathogenic T(H)2/T(H)17 cells i

107 poA-IV prevented airway hyperresponsiveness (AHR) and airway eosinophilia in mice following allergen

108 We determined airway hyperresponsiveness (AHR) and pulmonary inflammation by histologic and flow c

109 hallenge blunted airway hyperresponsiveness (AHR) and reduced fibronectin mRNA expression in ASM laye

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

111 are mediators of airway hyperresponsiveness (AHR) in asthma, however, mechanisms are not elucidated.

112 neutrophilia and airway hyperresponsiveness (AHR) in COPD patients.

113 , which leads to airway hyperresponsiveness (AHR) to contractile stimuli and airway obstruction.

114 weeks increases airway hyperresponsiveness (AHR) to methacholine challenge in C57BL/6J mice in assoc

115 n the lungs, and airway hyperresponsiveness (AHR) were examined.

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

117 thma is indirect airway hyperresponsiveness (AHR), and a prominent molecular endotype is the presence

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

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

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

121 We assessed airways hyperresponsiveness (AHR) and lung inflammation in germline and airway smooth

122 airway inflammation and hyperresponsiveness (AHR).

123 cretion, remodeling and hyperresponsiveness (AHR).

124 In summary, we identified AHR as a host factor for ZIKV replication and PML protei

125 Together, our experiments identify AHR signalling in enteric neurons as a regulatory node t

126 ne introgressed locus contains a deletion in AHR that confers a large adaptive advantage [selection c

127 2-3)/CC10 mice had a significant increase in AHR compared with wild-type mice.

128 Anakinra abolished an increase in AHR.

129 Increased nerve density resulted in AHR in vivo and in increased nerve-dependent airway reac

130 rmal human epidermal keratinocytes increased AHR binding in the gene regions of the glucose transport

131 We hypothesize that obesity increases AHR via the IL-1beta mechanism, which can be prevented b

132 0.001) and older age (per 1-year increment; AHR 1.06; 95% CI 1.02-1.10; p = 0.007).

133 strate that type 2 inflammation and indirect AHR in asthma are related to a shift in mast cell infilt

134 d with both type 2 inflammation and indirect AHR.

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

136 Allergen-induced AHR was unexpectedly diminished in Rgs4(-/-) mice, a fin

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

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

139 neutrophilia and had more severe CS-induced AHR.

140 tially protected mice from HDM + DEP induced AHR in association with decreased type 2 inflammation an

141 differential mechanisms govern FICZ-induced AHR signaling manifestations in HSCs versus LSCs.

142 The role of IL-33/ILC2 axis in RSV-induced AHR inflammation and eosinophilia were evaluated in the

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 We demonstrate that IDO-Kyn-AHR-mediated immunosuppression depends on an interplay b

146 onally, L. donovani activates IDO/kynurenine/AHR signaling in BMM s to maintain prolonged SOCS1 expre

147 8; p = 0.002), body mass index < 18.5 kg/m2 (AHR 3.65; 95% CI 1.73-7.72; p = 0.001) and older age (pe

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

149 ctivation by CpG A suppresses IL-33-mediated AHR and airway inflammation through inhibition of ILC2s.

150 pt in a preclinical model that FICZ-mediated AHR pathway activation enacts unique transcriptional pro

151 inhibiting the development of ILC2-mediated AHR.

152 Moreover, AHR supports transcriptional programs that promote ribos

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

154 ent to limit type 2 airway inflammation, not AHR.

155 f xenograft-bearing animals revealed nuclear AHR and upregulated TF and PAI-1 expression, telltale si

156 The ability of AHR to control expression of matrix metalloproteinase-1

157 In addition, activation of AHR by the endogenous ligand kynurenine inhibited cell p

158 ma, and that overexpression or activation of AHR offers a new therapeutic possibility for patients wi

159 ed ILC2s were crucial for the development of AHR and airway inflammation, during RSV infection.

160 significantly attenuated the development of AHR and decreased pulmonary accumulation of T(H)2/T(H)17

161 RGS4 may contribute to the development of AHR by reducing airway PGE2 biosynthesis in allergen- an

162 significantly attenuated the development of AHR in the setting of DEP-exacerbated allergic asthma an

163 IL-4, or IL-13, and inhibited development of AHR through contact-dependent suppression of helper CD4

164 rm HFD feeding attenuates the development of AHR, airway inflammation, pulmonary DC recruitment and M

165 tokines and contribute to the development of AHR.

166 hat suppressed the subsequent development of AHR.

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

168 In humans, the expression of AHR and CD39 was highest in grade 4 glioma, and high AHR

169 Microbiota-induced expression of AHR in neurons of the distal gastrointestinal tract enab

170 Expression of AHR-regulated gene CYP1A1 increased up to 41-fold and mo

171 ponses, and they highlight the importance of AHR signaling in mediating these responses.

172 rthermore, effects of coffee on induction of AHR- and Nrf2-pathway genes in Caco-2 cells were evaluat

173 Importantly, pharmacological inhibition of AHR activity suppressed TF and PAI-1 expression in endot

174 eview, we summarize our current knowledge of AHR and the transcriptional programmes it controls in th

175 te that TrkB signaling is a key modulator of AHR and that smooth muscle-derived BDNF mediates these e

176 sion in neuroblastoma, and overexpression of AHR downregulated MYCN expression, promoting cell differ

177 enograft model showed that overexpression of AHR significantly suppressed neuroblastoma tumor growth.

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

179 re, we further investigated the potential of AHR to serve as a prognostic indicator or a therapeutic

180 Finally, we discuss the role of AHR in autoimmune and neoplastic diseases of the central

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

182 rosclerosis to better understand the role of AHR in vascular disease.

183 A core set of AHR targets are uniquely repressed in LSCs across divers

184 First, the clinical significance of AHR in neuroblastoma was examined.

185 ice, occupancy of SHP is reduced and that of AHR is modestly increased at the miR-802 promoter, consi

186 onstantly exposed to many different types of AHR ligands, this has far-reaching implications for how

187 This phenotype is dependent on AHR in Tek-expressing radioresistant cells.

188 of normal vitamin D status had no effect on AHR once asthma was already established.

189 th AHR-competent Hepa1-GFP hepatoma cells or AHR-deficient LLC lung cancer cells.

190 correlate with neutrophilic inflammation or AHR.

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

192 ated inversely with the dose of piperaquine: AHRs (95% CI) for every 5-mg/kg increase 0.63 (0.48-0.84

193 Positive AHR immunostaining strongly correlated with differentiat

194 =45 ml or TRF >=50% had the worst prognosis (AHR: 2.26; 95% CI: 1.36 to 3.76; p = 0.002 for TRVol and

195 e of T-helper 2 (Th2) cytokines that promote AHR and lung inflammation.

196 We therefore propose AHR to be a novel disease gene for a new, recessively in

197 3%, 95% CI 7.1-12.2): adjusted hazard ratio (AHR) 12.63 (95% CI 6.40-24.92), p < 0.001.

198 lower risk of death [adjusted hazard ratio (AHR) = 0.58, 95% CI: 0.44-0.77] when compared to the ART

199 t population, with an adjusted hazard ratio (AHR) of 0.5 (95% CI 0.4-0.7, p < 0.001) and 0.3 (95% CI

200 ompensated cirrhosis (adjusted hazard ratio [AHR] 23.68; 95% CI 3.23-173.48; p = 0.002), body mass in

201 ion within 12 months (adjusted hazard ratio [AHR] = 5.0 [95% confidence interval (CI): 3.4-7.3], P <

202 relapse periodicity (adjusted hazard ratio [AHR] = 6.2, 95% CI 2.0-19.5; p = 0.002); patients treate

203 V function, both TRF (adjusted hazard ratio [AHR] per 10% increment: 1.26; 95% CI: 1.10 to 1.45; p =

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

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

206 ients (2.4% vs. 2.2%, adjusted hazard ratio [AHR]: 1.11; 95% confidence interval [CI]: 0.93 to 1.32).

207 nfection triggers aryl hydrocarbon receptor (AHR) activation.

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

209 y correlated with aryl hydrocarbon receptor (AHR) expression in neuroblastoma, and overexpression of

210 nscription factor aryl hydrocarbon receptor (AHR) functions as a biosensor in intestinal neural circu

211 T;p.Q621*) in the aryl hydrocarbon receptor (AHR) gene that perfectly co-segregated with the disease

212 a cells activates aryl hydrocarbon receptor (AHR) in TAMs to modulate their function and T cell immun

213 The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that int

214 The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor.

215 The Aryl hydrocarbon receptor (AHR) is an environment-sensing transcription factor that

216 The aryl hydrocarbon receptor (AHR) is expressed by immune cells and binds numerous xen

217 of miR-802 by aromatic hydrocarbon receptor (AHR) is inhibited by SHP.

218 The prototypical aryl hydrocarbon receptor (AHR) ligand, 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD),

219 We identified the aryl hydrocarbon receptor (AHR) pathway as a potent tumour suppressor in a SHH medu

220 ile repression of aryl hydrocarbon receptor (AHR) signaling has been shown to promote short-term main

221 h inducibility of aryl hydrocarbon receptor (AHR) signaling.

222 es are ligands of aryl hydrocarbon receptor (AHR) signaling.

223 nscription factor aryl hydrocarbon receptor (AHR) to drive the generation of Tregs and tolerogenic my

224 of activating the aryl hydrocarbon receptor (AHR) to limit ECM accumulation in vitro.

225 so identified the aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor widely inv

226 ignal through the aryl hydrocarbon receptor (AHR), a transcription factor with immunomodulatory funct

227 nscription factor aryl hydrocarbon receptor (AHR).

228 associated allelic homologous recombination (AHR) may well be a common mechanism driving (atypical) d

229 oth muscle-specific deletion of BDNF reduced AHR and blunted airway fibrosis but did not significantl

230 HH medulloblastomas characterised by reduced AHR pathway activity.

231 ogether, these findings suggest that reduced AHR pathway activity promotes SHH medulloblastoma progre

232 creased type 2 inflammation without reducing AHR.

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

234 of recent selection harbor genes regulating AHR signaling.

235 re, LSCs suppressed a set of FICZ-responsive AHR target genes that function as tumor suppressors and

236 also suppressed airway hyper-responsiveness (AHR) in terms of airway resistance and compliance to met

237 nflammation and airway hyper-responsiveness (AHR) with minimal pulmonary adverse reaction.

238 Airway hyper-responsiveness (AHR), pulmonary inflammation, and T-cell subsets were as

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

240 Selective AHR blockade delays progression in IDO/TDO-overexpressin

241 her sputum neutrophil counts and more severe AHR in COPD patients.

242 Here, we show AHR signaling is repressed in human AML blasts and prefe

243 ailed to upregulate a prominent LSC-specific AHR target in HSPCs, suggesting that differential mechan

244 o and in vivo administration of the specific AHR agonist FICZ significantly impaired leukemic growth,

245 OVA challenge, CD-fed mice developed strong AHR and airway inflammation, which were markedly reduced

246 In summary, AHR and CD39 expressed in TAMs participate in the regula

247 and that some subsets of NKT cells suppress AHR.

248 s and the therapeutic potential of targeting AHR in neurological disorders.

249 Overall, we conclude that AHR promotes the maintenance of lesion cap integrity and

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

251 We found that AHR knockdown reduced lactate, S-lactoylglutathione, N-a

252 obtained RNA sequencing data, we found that AHR mediates the expression of the UMP-generating enzyme

253 We hypothesized that AHR can affect atherosclerosis by regulating phenotypic

254 Our results indicate that AHR contributes to the regulation of metabolic pathways

255 In conclusion, our results indicate that AHR is a novel prognostic biomarker for neuroblastoma, a

256 These results indicate that AHR up-regulates sphingolipid levels and is important fo

257 We propose that AHR is likely protective based on these data and inferen

258 red human coronary artery SMCs revealed that AHR modulates the human coronary artery SMC phenotype an

259 These findings show that AHR may function as a tumor suppressor in childhood neur

260 Taken together, these studies suggest that AHR activation could be a promising target to block exce

261 Previous studies suggest that AHR ligands alter cholesterol homeostasis in mice throug

262 The AHR is an environmental sensor and transcription factor

263 The AHR ligand, 6-formylindolo[3,2b]carbazole (FICZ) was use

264 The AHR pathway is suppressed in leukemic stem cells (LSC),

265 The AHR was 7.8 (95% CI: 5.0-12.3) for P. vivax and 3.0 (95%

266 2b]carbazole (FICZ) was used to activate the AHR pathway in OFs.

267 rom the xenograft-bearing mice activated the AHR pathway and augmented tissue factor (TF) and plasmin

268 rly life exposure to chemicals that bind the AHR impairs CD4(+) T cell responses to influenza A virus

269 Our findings suggest that blocking the AHR pathway in IDO/TDO expressing tumors would overcome

270 ld-type and muMT mice developed AHR, but the AHR was significantly stronger in muMT mice, as confirme

271 Glycolysis was lowered by activation of the AHR as measured by decreases in glucose uptake and the p

272 These data show that activation of the AHR by FICZ increases MMP1 expression while leading to a

273 f the ENO1 promoter showed activation of the AHR decreases the transcription of ENO1.

274 The prototypical ligand of the AHR is an environmental contaminant called 2,3,7,8-tetra

275 soriasis displayed reduced activation of the AHR pathway and increased CYP1A1 enzymatic activity comp

276 Activation of the AHR pathway downmodulates skin inflammatory responses in

277 ammatory effect exerted by activation of the AHR pathway in the skin.

278 medulloblastomas with high expression of the AHR repressor (AHRR) exhibited a significantly worse pro

279 differentiation, and that activation of the AHR, by lowering the expression of SLC2A1 and ENO1, can

280 n of glycolysis, either by activation of the AHR, inhibition of glucose transport, or inhibition of e

281 cose metabolism, either by activation of the AHR, inhibition of glycolysis, inhibition of glucose tra

282 een these metabolites and the control of the AHR-TF/PAI-1 axis and VTE in cancer.

283 donors, suggesting that dysregulation of the AHR/CYP1A1 axis may play a role in inflammatory skin dis

284 Here, we show that the AHR pathway is selectively active in IDO/TDO-overexpress

285 ed both AHR and ARNT, demonstrating that the AHR-ARNT transcriptional complex is necessary for expres

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

287 Thus, AHR is necessary for the proliferation of MYC-overexpres

288 type 2 inflammation and its relationship to AHR are incompletely understood.

289 ere, we investigated enterocyte responses to AHR agonists in coffee and measured their transport acro

290 3-activated ILC2s in mediating RSV-triggered AHR and eosinophilia.

291 Moreover, ZIKV-triggered AHR activation suppresses intrinsic immunity driven by t

292 lic pathways were associated with triggering AHR during development.

293 95% CI: 1.10 to 1.45; p = 0.001) and TRVol (AHR per 10-ml increment: 1.15; 95% CI: 1.04 to 1.26; p =

294 the metabolome of MYC-expressing cells upon AHR knockdown.

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

296 A (LDHA), establishing a mechanism by which AHR regulates lactate and UMP production in MYC-overexpr

297 To define metabolic pathways in which AHR cooperates with MYC in supporting cell growth, here

298 KISS1 expression positively correlated with AHR, and high KISS1 expression predicted better survival

299 ncreased chromatin binding corresponded with AHR-dependent decreases in levels of SLC2A1 and ENO1 mRN

300 d with TCDD and injected subcutaneously with AHR-competent Hepa1-GFP hepatoma cells or AHR-deficient