ライフサイエンスコーパス: TCDD

1 TCDD (dioxin) induces a rapid inflammatory response from

2 TCDD activates the aryl hydrocarbon receptor, a transcri

3 TCDD also disrupted expression of other genes involved i

4 TCDD also increased acetylation and ubiquitin-dependent

5 TCDD also increased cytosolic [Ca(2+)](c) and RyR1-speci

6 TCDD and 8 of the PAHs induced EROD activity in a concen

7 TCDD concentration in 1976 was inversely associated with

8 TCDD concentrations were measured in 1976 (n = 981) and

9 TCDD cotreatment inhibited EE-induced uterine wet weight

10 TCDD exposure was not associated with levels of other th

11 TCDD exposure, particularly exposure before menarche, ma

12 TCDD inhibited mouse hs1,2 similarly to the mouse 3'IghR

13 TCDD inhibits mouse 3'IghRR activation and induces aryl

14 TCDD is a potent activator of the aryl hydrocarbon recep

15 TCDD suppressed hepatic glucose production, expression o

16 TCDD treatment to mice increased the numbers of phenotyp

17 TCDD+Endosulfan elicit a complex signaling sequence invo

18 TCDD-CD4(+) cells also secrete significant amounts of IL

19 TCDD-CD4(+) cells demonstrated an increased responsivene

20 TCDD-EQs calculated for endangered populations of white

21 TCDD-mediated apoptosis in activated peripheral T cells

22 s strengthened the relationship between 1976 TCDD and total thyroxine but drove the association with

23 DD were slightly weaker than those with 1976 TCDD.

24 between total thyroxine and concurrent 1996 TCDD were slightly weaker than those with 1976 TCDD.

25 hyroxine but drove the association with 1996 TCDD to the null.

26 e analysis (1977-2014) of 2378-TCDF and 2378-TCDD raw concentrations in Lake Ontario lake trout revea

27 itions, the reaction between O2(-*) and 2378-TCDD results in structure diagnostic cleavages of the C-

28 s 2,3,7,8-tetrachloro-dibenzo-p-dioxin (2378-TCDD), a compound reputed as one of the most toxic chemi

29 ately 5 fg and 10 fg, respectively, for 2378-TCDD and 5-10 fg and 10-30 fg, respectively, for the 2,3

30 essure chemical ionization (APCI(-)) of 2378-TCDD was described in this journal over 30 years ago.

31 tivated by DLCs with EC50 values for 2,3,7,8-TCDD that are lower than those of any other AhR of verte

32 For standard solutions of 2,3,7,8-TCDD, injections of 10 fg in the splitless mode on 30- o

33 ations of three agonists of the AHR, 2,3,7,8-TCDD, PCB 77, and benzo[a]pyrene, in livers of a nonmode

34 Emissions of 2,3,7,8-TCDD, the most toxic congener (TEF = 1.0), increased 320

35 Emissions of 2,3,7,8-TCDD, the most toxic congener [toxicity equivalence fact

36 o a downstream posttranslational change in a TCDD target protein (PEPCK), and 3) reveals that the AHR

37 in cannot transactivate the Ah receptor in a TCDD-dependent fashion.

38 The results reveal that TiPARP can mediate a TCDD effect, that the AHR is linked to PGC1alpha functio

39 ibose) polymerase, PARP7) that can mediate a TCDD toxicity, i.e. suppression of hepatic gluconeogenes

40 expression alone was sufficient to produce a TCDD-like jaw phenotype.

41 d binding cavity necessary for high-affinity TCDD binding and TCDD-dependent AhR transformation DNA b

42 ly decreased in WT and mutant cultures after TCDD treatment.

43 sponse in the developing zebrafish jaw after TCDD exposure using DNA microarrays.

44 All TCDD toxicities require activation of the aryl hydrocarb

45 ription factor that mediates most if not all TCDD responses.

46 P) 1A, main AHR-induced genes, did not alter TCDD suppression of gluconeogenesis.

47 blunted reporter activity but did not alter TCDD's effect (i.e., no shift from activation to inhibit

48 We concluded that although TCDD may be affecting the expression of some genes gover

49 nship between gene activation by the AHR and TCDD toxicities is not well understood.

50 Cyp1b1/CYP1B1, AhR repressor (Ahrr/AhRR) and TCDD-inducible poly(ADP-ribose)polymerase (Tiparp/TiPARP

51 BaP and TCDD enhanced osteoclast formation in bone marrow cell c

52 necessary for high-affinity TCDD binding and TCDD-dependent AhR transformation DNA binding.

53 Both endosulfan and TCDD are persistent organic pollutants which elicit cyto

54 AhR expression and TCDD-mediated induction of CYP1A1 was significantly redu

55 d polycyclic aromatic hydrocarbon (PAH)- and TCDD-induced reporter activity by 75% and 90% respective

56 y use of TEFs for fishes used by the WHO and TCDD equivalents (TCDD-EQs) via the use of RePs for AhR2

57 is not known how AHR activation produces any TCDD toxicity.

58 exposure to persistent AhR agonists, such as TCDD (dioxin, 2,3,7,8-tetrachlorodibenzo-p-dioxin).

59 n is disrupted by exogenous ligands, such as TCDD, to induce G(1) cell cycle arrest.

60 Because TCDD causes craniofacial malformations in zebrafish by d

61 med ratio measure of the association between TCDD and DM.

62 gic evidence suggests an association between TCDD and metabolic disease.

63 Here, we evaluated the association between TCDD exposure and bone structure and geometry in adultho

64 insensitive to dioxin, and Xenopus AHRs bind TCDD with low affinity.

65 as compared to widespread AHR2-2 in binding TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) and in drivin

66 and function indicate that axolotl AHR binds TCDD weakly, predicting that A. mexicanum lacks sensitiv

67 sox9b mRNA and then exposed to TCDD blocked TCDD-induced jaw toxicity in approximately 14% of sox9b-

68 The human AhR bound TCDD with significantly lower affinity than the rat AhR.

69 contribution to hu-hs1,2 basal activity, but TCDD-induced activity was not strictly IS number depende

70 in 14, were inhibited by greater than 90% by TCDD.

71 In contrast, hu-hs1,2 was activated by TCDD, and antagonist studies supported an aryl hydrocarb

72 Our findings indicate that AHR activation by TCDD in the fetus during pregnancy leads to impairment o

73 Furthermore, developmental AHR activation by TCDD increased ROS in the fetal hematopoietic stem cells

74 in-o-deethylase (EROD) enzymatic activity by TCDD.

75 mmetry whose expression would be affected by TCDD.

76 Activation of AhR by TCDD caused a significant increase of the inflammatory c

77 on mediated through activation of the AhR by TCDD may represent a novel pathway for the induction of

78 Comparison of transcripts altered by TCDD in jaw with transcripts altered in embryonic heart

79 e in sox9b expression in the heart caused by TCDD plays a role in many of the observed signs of cardi

80 adduct formation and DNA damage elicited by TCDD or benzo[a]pyrene.

81 rthermore, the osteoclastogenesis induced by TCDD was lower in Cyp1a1/1a2(-/-) and Cyp1a1/1a2/1b1(-/-

82 2 mRNA expression is dramatically induced by TCDD.

83 than male mice to acute toxicity induced by TCDD.

84 h may protect from acute toxicity induced by TCDD.

85 A in Hepa-1 cells enhanced EROD induction by TCDD and efficiently rescued TCDD induction of EROD acti

86 classical mechanisms of UGT1A1 induction by TCDD.

87 increased sensitivity to jaw malformation by TCDD.

88 hondrogenic transcripts were misregulated by TCDD in the jaw.

89 onstrates that inhibition of regeneration by TCDD is mediated by misinduction of R-Spondin1.

90 to further characterize these CD4(+) cells (TCDD-CD4(+) cells) by comparing and contrasting them wit

91 In addition, siRNAs for SIN3A decreased TCDD-mediated induction of CYP1A1 mRNA and EROD activity

92 esulted from direct effects of developmental TCDD exposure on CD4+ T cells.

93 nd pure 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (normalized at 0.1 mug/kg TEQ) and acquired plasma

94 2 ng/kg 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (range: 15-672), which is equivalent to 75% (range

95 tudies, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) alters glucose transport and increases serum lipid

96 The potency of tetrachlorodibenzo-p-dioxin (TCDD) and 18 polycyclic aromatic hydrocarbons (PAHs) for

97 ved for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and also microbiota-derived AhR ligands tryptamine

98 nts for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and other dioxins rely on estimates of elimination

99 vels of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and the occurrence of diabetes mellitus (DM), and

100 ects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) are mediated through binding and activation of the

101 agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) compromises the competitive reconstitution of bone

102 ects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure.

103 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) impairs craniofacial skeletal development across m

104 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) induces nonobstructive hydronephrosis in mouse neo

105 aP) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) interact with the aryl hydrocarbon receptor (Ahr)

106 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a persistent environmental contaminant which el

107 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a persistent environmental contaminant.

108 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is an environmental toxicant known to inhibit Ab s

109 sure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is based upon the identities of the amino acids at

110 agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) leads to a significant decline in the percentage o

111 ects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on T cells in vivo have been well characterized, a

112 ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the expression of cytochrome P450 (CYP)1A1 and

113 ptor by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) prevents the formation of the epicardium and leads

114 AHR) by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) prevents the proper formation of craniofacial cart

115 uced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) via the aryl hydrocarbon receptor.

116 Ps) of 2,3,7,8-tetrachloro-dibenzo-p-dioxin (TCDD), 2,3,4,7,8-pentachloro-dibenzofuran, 2,3,7,8-tetra

117 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a widespread environmental contaminant, is a know

118 , e.g., 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), activate the aryl hydrocarbon receptor (AhR), cau

119 cluding 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), causes a wide array of toxicities in vertebrates,

120 onist, 2,3,7,8-tetracholorodibenzo-p-dioxin (TCDD), causes increases in both hepatocytic and cholangi

121 such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), has more recently attracted the attention of immu

122 ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), in utero and via suckling.

123 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), is primarily produced via industrial processes in

124 ioxins [2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), polychlorinated dibenzo-p-dioxins (PCDDs)], furan

125 ceptor, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), produced a similar induction of P-glycoprotein, w

126 nhibited 2,3,7,8-tetrachlordibenzo-p-dioxin (TCDD)-induced cytochrome P450 (CYP) enzyme activity and

127 of AhR induced tetrachlorodibenzo-p-dioxin (TCDD)-inducible poly(ADP-ribose) polymerase (TiPARP) gen

128 nhanced 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-mediated induction of CYP1A1 in thymus of B6 mice.

129 agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

130 aminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

131 ]P) and 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD).

132 such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

133 ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

134 cinogen 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

135 onist, 2,3,7,8-tetra-chlorodibenzo-p-dioxin (TCDD).

136 ved for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

137 ity for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

138 or AhR [2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)], CAR [6-(4-chlorophenyl)imidazo[2,1-b][1,3]thiazo

139 cinogen 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin) include a wasting syndrome associated with

140 t binds 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin).

141 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD, or dioxin) is known to induce rapid inflammatory c

142 nitive hematopoiesis (treatment with dioxin (TCDD), and injection of an antisense morpholino oligonuc

143 Dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin, TCDD) is a carcinogenic and highly toxic industrial bypr

144 dioxin (2,3,7,8-tetrachlorodibenzo[p]dioxin, TCDD) to promote epigenetic transgenerational inheritanc

145 ere concentrations of the most toxic dioxin, TCDD, are about 2 orders of magnitude higher than at the

146 dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin; TCDD).

147 ages of the C-O bonds, which can distinguish TCDD isomers on the basis of Cl distribution between the

148 e AhRR Tg mice were protected from high-dose TCDD-induced lethality associated with a reduced inflamm

149 paB) repressed both normal and LPS-enhanced, TCDD-inducible, AhR-dependent gene expression and canoni

150 fishes used by the WHO and TCDD equivalents (TCDD-EQs) via the use of RePs for AhR2 of white sturgeon

151 ly lower in AhRR Tg versus wt mice following TCDD treatment.

152 ngeners in all three species was as follows: TCDD>dibenz[ah]anthracene>benzo[k]fluoranthene>indeno[1,

153 between 2002 and the time of blood draw for TCDD measurement (adjusted OR, 2.37; 95% CI, 1.27-4.44;

154 and in transactivation assays, the EC50 for TCDD was 23 nM, similar to X. laevis AHR1beta (27 nM) an

155 gap in species sensitivity was 100-fold for TCDD, and generally </=10-fold for PAHs.

156 entration-dependent toxicokinetic models for TCDD underpredicted observed elimination rates for conce

157 The median (range) for TCDD was 2.9 (0.4-12.1) pg/g lipid and PCDD TEQ was 8.7

158 We demonstrate that SIN3A is required for TCDD induction of the CYP1A1 protein in Hepa-1 cells but

159 of R-Spondin/LRP6 is absolutely required for TCDD to inhibit fin regeneration.

160 a novel protein-DNA complex responsible for TCDD-inducible expression.

161 with a composite half-life of 9.3 years for TCDD toxic equivalents.

162 Brain capillaries from TCDD-dosed rats (1-5 mug/kg, i.p.) exhibited increased t

163 -glycoprotein expression in capillaries from TCDD-dosed rats, in situ brain perfusion indicated signi

164 However, TCDD-mediated Cyp1A1 induction in the mammary glands of

165 lts suggest that reduced sox9b expression in TCDD-exposed zebrafish embryos contributes to jaw malfor

166 The reduction of sox9b expression in TCDD-exposed zebrafish embryos has been shown to contrib

167 ral genes were significantly up-regulated in TCDD-CD4(+) cells including TGF-beta3, Blimp-1, and gran

168 and is hypothesized to have a causal role in TCDD-induced toxicity.

169 hese differences often explain variations in TCDD toxicity.

170 treated with various AHR agonists including TCDD, 6-formylindolo-[3,2-b]carbazole (FICZ), and 3-3'-d

171 ailable data do not indicate that increasing TCDD exposure is associated with an increased risk of DM

172 Individual TCDD concentration was measured in archived serum collec

173 Individual TCDD concentration was measured in archived serum that h

174 tional studies of populations with low-level TCDD exposures (serum concentrations <10 pg/g lipid) and

175 n: NO-aspirin 2 inhibited binding of ligand (TCDD)-activated aryl hydrocarbon receptor to the CYP1A1

176 most active halogenated carbazoles and, like TCDD, contains 4 lateral substituents; however, the esti

177 alized, normal mammary epithelial cell line, TCDD rapidly activates the enzymatic activity of cytosol

178 ntical residues at positions that confer low TCDD affinity to X. laevis AHRs (A364, A380, and N335),

179 primary T cells cultured with 10 to 1000 nM TCDD were relatively resistant to apoptosis, they became

180 solated rat brain capillaries to 0.05-0.5 nM TCDD roughly doubled transport activity and protein expr

181 Significantly, CA but not TCDD induces expression of Stc2 in hepatocytes.

182 In summary, we identify a novel TCDD-responsive enhancer for CYP1A2.

183 Only 2% of TCDD-CD4(+) cells express Foxp3, suggesting that the AhR

184 ement of the nongenomic pathway of action of TCDD as shown previously in MCF10A cells.

185 This action of TCDD is clearly antagonized by cell pretreatment with AA

186 Such an action of TCDD is clearly blocked by methylarachidonyl fluorophosp

187 This early inflammatory action of TCDD is clearly different from that mediated by its clas

188 ing blockers, indicating that this action of TCDD is mediated by calcium-triggered activation of cPLA

189 This action of TCDD is quite different from the classic action of TCDD

190 at the influence of the nongenomic action of TCDD lasts a long time in this cell material.

191 ent from the conventional model of action of TCDD through the "genomic" pathway.

192 s quite different from the classic action of TCDD to induce cytochrome P450 1A1 (CYP1A1) because bloc

193 s support the model that the early action of TCDD to induce rapid inflammatory responses is carried o

194 sting influence of this nongenomic action of TCDD, we tested the effects of AACOCF3, exogenous arachi

195 (an inhibitor of PKA) on the 5 day action of TCDD.

196 rly antagonized all the long-term actions of TCDD except that on CYP1A1 induction, indicating that th

197 derstanding of the molecular determinants of TCDD binding and provide a basis for future studies dire

198 Docking of TCDD to sets of consensus models of killifish, rat, and

199 xpression caused by three different doses of TCDD (2,3,7,8-tetracholorodibenzo-p-dioxone).

200 The present study examined the effect of TCDD exposure on liver regeneration following 70% partia

201 Such an inflammatory effect of TCDD on 3T3-L1 adipocyes persists at least for 5 days, w

202 R-Spondin1 reversed the inhibitory effect of TCDD, and tissue regeneration was restored.

203 phenocopy many but not all of the effects of TCDD at the heart.

204 Therefore, the effects of TCDD on ethynyl estradiol (EE)-mediated uterine gene exp

205 l line (CH12.LX), we compared the effects of TCDD on mouse hs1,2 versus hu-hs1,2 activity.

206 Our findings suggested that the effects of TCDD on the developing hematopoietic system were mediate

207 liver damage as indicated by lower levels of TCDD-induced alanine aminotransferase and hepatic trigly

208 the presence of DCs showed highest levels of TCDD-induced apoptosis.

209 Here, we show that the loss of TCDD-inducible poly(ADP-ribose) polymerase (Tiparp), an

210 Sublethal concentrations of mixtures of TCDD and endosulfan increase oxidative stress, as well a

211 possibly contributing to slower oxidation of TCDD.

212 CCND1 complex was reduced in the presence of TCDD.

213 Higher quartiles of TCDD and PCDD TEQs were associated with lower sperm conc

214 uated using molecular docking simulations of TCDD with both wild-type and mutant mAhRs.

215 est that hu-hs1,2 is a significant target of TCDD and support species differences in hs1,2 regulation

216 adulthood, and considered whether timing of TCDD exposure before achievement of peak bone mass (assu

217 e, the inhibitory effects of NO-aspirin 2 on TCDD-induced CYP activity and mRNA expression were consi

218 e, aspirin alone had no inhibitory effect on TCDD-induced CYP activity, nor did aspirin up-regulate G

219 However, VPA- or TCDD-induced P-glycoprotein transport was blocked in the

220 of results for low current versus high past TCDD levels, the available data do not indicate that inc

221 do not support the hypothesis that postnatal TCDD exposure adversely affects adult bone health.

222 ve studies of persons with high prediagnosis TCDD body burdens.

223 3 constituent, nicotinamide (NAM), prevented TCDD suppression of glucose output, NAD(+), and gluconeo

224 Like natural T-regs, TCDD-CD4(+) cells do not produce IL-2 and their suppress

225 TiPARP overexpression reproduced TCDD effects on glucose output and NAD(+) levels whereas

226 OD induction by TCDD and efficiently rescued TCDD induction of EROD activity in cells treated with an

227 Serum TCDD levels were measured in 1987, 1992, 1997, and 2002.

228 The dose-response relationship between serum TCDD and DM across studies was examined using 2 dependen

229 A 10-fold increase in serum TCDD (log10TCDD) was not associated with diabetes (adjus

230 the women, we examined the relation of serum TCDD to diabetes, metabolic syndrome, and obesity > 30 y

231 Higher peripubertal serum TCDD concentrations and PCDD TEQs were associated with p

232 The highest quartile of peripubertal serum TCDD concentrations was associated with a decrease (95%

233 Specifically, TCDD elicited a >200-fold increase in taurolithocholic a

234 In animal studies, TCDD exposure impairs bone metabolism and increases frag

235 ntal toxin 2,3,7,8-tetrachlorodibenzodioxin (TCDD) is a known human carcinogen; however, its precise

236 nown POPs [2,3,7,8-tetrachlorodibenzodioxin (TCDD), 2,2 ,4,4 ,5,5 -hexachlorobiphenyl (PCB 153), and

237 n elimination rates for congeners other than TCDD.

238 most potent DLC, PeCDF was more potent than TCDD at activating Japanese quail (13- to 26-fold) and c

239 eveloping zebrafish heart ventricle and that TCDD exposure markedly reduces this expression.

240 Contrary to the assumption that TCDD is the most potent DLC, PeCDF was more potent than

241 with AhR expression constructs confirm that TCDD-inducibility is AhR-dependent and requires direct A

242 , and p27(Kip1) knockout mice confirmed that TCDD-induced inhibition of liver regeneration is entirel

243 We establish that TCDD treatment of Hepa-1 cells rapidly increases the deg

244 We found that TCDD-CD4(+) cells actively proliferate in response to va

245 We report here that TCDD-induced TiPARP also targets PEPCK for ADP-ribosylat

246 In this study, we tested the hypothesis that TCDD-mediated phenotypic and functional changes of HSCs

247 Taken together, these results reveal that TCDD may promote tumor progression in vivo by directly t

248 tive to TCDD-induced apoptosis revealed that TCDD treatment of activated but not nonactivated T cells

249 Using organ culture experiments we show that TCDD also represses Smoc2 mRNA expression in testes from

250 Here we show that TCDD induces mitochondrial dysfunction, stress signaling

251 K506, and CnA mRNA silencing suggesting that TCDD triggers a signaling pathway similar to mtDNA deple

252 Although experimental evidence suggests that TCDD alters thyroid hormone levels in rodents, human dat

253 t study demonstrates for the first time that TCDD can induce apoptosis in vitro in peripheral T cells

254 21(Cip1) expression completely abrogated the TCDD inhibition, and accelerated hepatocyte progression

255 enes are novel targets for modulation by the TCDD-activated AHR and may be involved in the observed c

256 as associated with a reduced capacity of the TCDD-exposed fetal cells to compete with control cells i

257 Axolotl AHR bound one-tenth the TCDD of mouse AHR in velocity sedimentation analysis, an

258 We hypothesized that the TCDD reduction of sox9b expression plays an integral rol

259 eptor LRP6, we further demonstrated that the TCDD-mediated block in regeneration is also LRP6 depende

260 ing to the onset of hydronephrosis using the TCDD-exposed mouse model will deepen our understanding o

261 nal analysis, have allowed detection of the "TCDD binding-fingerprint" of conserved residues within t

262 pathway by which the AHR target gene TiPARP (TCDD-inducible poly(ADP-ribose) polymerase) contributes

263 r the first time an AHR target gene, TiPARP (TCDD-inducible poly(ADP-ribose) polymerase, PARP7) that

264 ffect potency for this compound (compared to TCDD) was 0.0001 and 0.0032, based on induction of CYP1A

265 In contrast to TCDD, CA is unable to induce the CYP1A1 gene, thus revea

266 poly(ADP-ribose) polymerase) contributes to TCDD suppression of transcription of phosphoenolpyruvate

267 Zebrafish larvae were exposed to TCDD at 96 h after fertilization, and jaw cartilage tiss

268 injected with sox9b mRNA and then exposed to TCDD blocked TCDD-induced jaw toxicity in approximately

269 Mice exposed to TCDD during an acute B6-into-B6D2F1 graft-vs-host respon

270 that had not been developmentally exposed to TCDD.

271 Exposure to TCDD caused a rapid accumulation of neutrophils and macr

272 Exposure to TCDD induces acute thymocyte cell loss, which occurs con

273 Maternal exposure to TCDD resulted in durable changes in the responsive capac

274 in the highest known residential exposure to TCDD.

275 in the highest known residential exposure to TCDD.

276 d that both adult and larval fins respond to TCDD during regeneration with misexpression of Wnt signa

277 , whereas activated T cells are sensitive to TCDD-induced apoptosis revealed that TCDD treatment of a

278 nonactivated T cells made them sensitive to TCDD-induced apoptosis.

279 ne whether hu-hs1,2 activity is sensitive to TCDD.

280 ed species differences in AhR sensitivity to TCDD and understanding the mechanistic basis for the dra

281 i) the sensitivity of other avian species to TCDD, 2,3,4,7,8-pentachlorodibenzofuran (PeCDF), and 2,3

282 ive T cells from C57BL/6 mice susceptible to TCDD-induced apoptosis in vitro.

283 ors from fetuses exposed transplacentally to TCDD were mixed 1:1 with cells from congenic controls an

284 The environmental toxin TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin, dioxin) produ

285 es to identify the effects of transplacental TCDD on AHR activation in the fetus.

286 ycle, and the interaction was disrupted upon TCDD treatment.

287 Weak TCDD binding results from the combination of three resid

288 to determine whether this mechanism of weak TCDD binding is shared by other amphibian AHRs.

289 l killer (cNK) cell differentiation, whereas TCDD treatment blocked cNK development and supported gro

290 alence of metabolic syndrome associated with TCDD, but only among women who were the youngest at the

291 Treatment of C2C12 cells with TCDD disrupted mitochondrial transmembrane potential in

292 In addition, DC maturation and culture with TCDD caused significant induction of FasL.

293 Male C57BL/6 mice orally gavaged with TCDD (0.01-30 microg/kg) every 4 days for 28 days exhibi

294 Cells treated with TCDD displayed resistance to apoptosis, increased expres

295 e assays in AHR-deficient cells treated with TCDD or PCB126.

296 By contrast, treatment with TCDD resulted in a rapid loss of viability of rHBs, even

297 adipose tissue of mice after treatment with TCDD using flow cytometry.

298 Compared with that for women with TCDD levels of < or = 20 parts per trillion, the age-adj

299 In contrast, among postmenopausal women, TCDD levels were associated with evidence of better bone

300 Among premenopausal women, TCDD serum levels were associated with some indexes indi