ライフサイエンスコーパス: TCDD

1 TCDD activates the aryl hydrocarbon receptor, a transcri

2 TCDD administration in naive mice also led to induction

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 diminished the rhythmicity of several core clock re

10 TCDD exposure is associated with many adverse health out

11 TCDD exposure was not associated with levels of other th

12 TCDD exposure, particularly exposure before menarche, ma

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

14 TCDD inhibits mouse 3'IghRR activation and induces aryl

15 TCDD is a potent activator of the aryl hydrocarbon recep

16 TCDD reduced the growth rates of the resulting tumors in

17 TCDD suppressed hepatic glucose production, expression o

18 TCDD treatment to mice increased the numbers of phenotyp

19 TCDD+Endosulfan elicit a complex signaling sequence invo

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

21 TCDD-EQs calculated for endangered populations of white

22 TCDD-induced MDSCs had high mitochondrial respiration an

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

24 DD were slightly weaker than those with 1976 TCDD.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

43 All TCDD toxicities require activation of the aryl hydrocarb

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

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

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

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

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

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

50 s 27 and 57 part per billion toward BCDD and TCDD, respectively, and is very selective as well withou

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

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

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

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

55 Simvastatin and TCDD (S + T) co-treatment increased hepatic AHR-battery

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 pounds from environmental toxicants, such as TCDD, that are carcinogenic to dietary indoles that are

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

61 Because TCDD causes craniofacial malformations in zebrafish by d

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 The responses elicited by TCDD were associated with effects on tumor vascularity,

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

80 than male mice to acute toxicity induced by TCDD.

81 h may protect from acute toxicity induced by TCDD.

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

83 increased sensitivity to jaw malformation by TCDD.

84 hondrogenic transcripts were misregulated by TCDD in the jaw.

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

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

87 Simvastatin exposure decreased TCDD-induced hepatic lipid accumulation in both sexes, b

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

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

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

91 2 ng/kg 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (range: 15-672), which is equivalent to 75% (range

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

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

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

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

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

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

98 ed with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) every 4 days for 28 days.

99 pact of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure, a ubiquitous and highly toxic pollutant,

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

101 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) induces nonobstructive hydronephrosis in mouse neo

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

103 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a persistent environmental contaminant which el

104 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a persistent environmental contaminant.

105 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is an environmental toxicant known to inhibit Ab s

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

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

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

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

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

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

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

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

114 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a persistent environmental contaminant, induces s

115 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a widespread environmental contaminant, is a know

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

117 ompound 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), an environmental contaminant, is a potent ligand

118 ions of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), an environmental contaminant, primarily depend on

119 DD) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), based on the fluorescence quenching.

120 bind to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), but stronger binding to gmAhr1a was observed.

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

122 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), for which the epidemiological evidence is mixed,

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

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

125 ligand, 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), induces CYP1 family enzymes, which can metabolize

126 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), is primarily produced via industrial processes in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

143 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD, or dioxin) is known to induce rapid inflammatory c

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

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

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

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

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

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

150 s to the upregulation of downstream effector TCDD-inducible poly(ADP-ribose) polymerase (TiPARP) duri

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

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

153 For example, TCDD flattened expression of the rate-limiting enzymes i

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

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

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

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

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

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

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

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

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

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

164 has identified VEGFR1 as a novel target for TCDD, which provides the basis for further elucidating t

165 1) could be one of the potential targets for TCDD in both mouse and humans.

166 identify novel protein receptor targets for TCDD using computational and in vitro validation experim

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

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

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

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

171 ntagonist in mice led to marked reduction in TCDD-induced MDSCs.

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

173 aracterize the impact of HMGCR repression in TCDD-induced liver injury.

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

175 hese differences often explain variations in TCDD toxicity.

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

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

178 Individual TCDD concentration was measured in archived serum collec

179 Individual TCDD concentration was measured in archived serum that h

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

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

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

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

184 In mice, TCDD treatment replicated many of the hallmark symptoms

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

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

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

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

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

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

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

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

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

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

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

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

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

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

199 tein and metabolite levels within context of TCDD-elicited progression of steatosis to steatohepatiti

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

201 hanged within 72 h following a bolus dose of TCDD.

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

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

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

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 udy, the time- and dose-dependent effects of TCDD were examined on hepatic OCM in mice.

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

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

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

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

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 glycogen metabolism and increase the risk of TCDD-elicited liver damage in a sex-specific manner.

215 he basis for further elucidating the role of TCDD in angiogenesis.

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

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

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

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

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

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

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

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

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

225 3 constituent, nicotinamide (NAM), prevented TCDD suppression of glucose output, NAD(+), and gluconeo

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

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

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

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

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

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

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

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

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

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

236 Collectively, these results suggest TCDD disrupted circadian regulation of hepatic metabolis

237 Upon systemic TCDD treatment, PAX3-negative MuSCs display impaired sur

238 nists like 2,3,7,8-tetrachlorodibenzodioxin (TCDD) and 6-formylindolo[3,2-b]carbazole (FICZ).

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

240 n elimination rates for congeners other than TCDD.

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

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

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

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

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

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

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

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

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

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

251 In vitro validation results showed that TCDD can bind and phosphorylate hVEGFR1.

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

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

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

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

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

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

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

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

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

267 C57BL/6 mice were exposed to TCDD in the presence or absence of simvastatin, a compet

268 that had not been developmentally exposed to TCDD.

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

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

271 in the highest known residential exposure to TCDD.

272 naive C57BL/6 mice that were exposed i.p. to TCDD showed massive mobilization of myeloid-derived supp

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

274 is one order of magnitude more sensitive to TCDD than gmAhr2a, but the maximal responses of the rece

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

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

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

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

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

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

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

282 n VEGFR1 (hVEGFR1) has less affinity towards TCDD compared to the mouse VEGFR1 (mVEGFR1).

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

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

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

286 Weak TCDD binding results from the combination of three resid

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

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

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

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

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

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

293 studies showed that hVEGFR1 interaction with TCDD is stable throughout the simulation time.

294 onists, the distinct binding properties with TCDD and BNF, and the distinct tissue-specific expressio

295 -rich or omega6-rich diets were treated with TCDD and injected subcutaneously with AHR-competent Hepa

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

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

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

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

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

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