ライフサイエンスコーパス: 2,3,7,8-tetrachlorodibenzo-p-dioxin

1 roteins, mediates the toxic effects of TCDD (2,3,7,8 tetrachlorodibenzo-p-dioxin).

2 rsistent AhR agonists, such as TCDD (dioxin, 2,3,7,8-tetrachlorodibenzo-p-dioxin).

3 inding species or affect activation by TCDD (2, 3,7,8-tetrachlorodibenzo-p-dioxin).

4 ose of the most potent dioxin-like compound, 2,3,7,8-tetrachlorodibenzo-p-dioxin.

5 e toxicologic and carcinogenic properties of 2,3,7,8-tetrachlorodibenzo-p-dioxin.

6 the environmental contaminant and AHR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin.

7 atoma cells to the microsomal enzyme inducer 2,3,7,8-tetrachlorodibenzo-p-dioxin.

8 l toxicants such as 3-methylcholanthrene and 2,3,7,8-tetrachlorodibenzo-p-dioxin.

9 augments the response of the CYP1A1 gene to 2,3,7,8-tetrachlorodibenzo-p-dioxin.

10 ntal contaminants such as benzo[a]pyrene and 2,3,7,8-tetrachlorodibenzo-p-dioxin.

11 m studies using the toxic synthetic chemical 2,3,7,8-tetrachlorodibenzo-p-dioxin.

12 l treatment with IL1beta and the AHR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin.

13 e of increased disease risk from exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin.

14 r that mediates the effects of agonists like 2,3, 7,8-tetrachlorodibenzo-p-dioxin.

15 ponses to environmental contaminants such as 2,3,7, 8-tetrachlorodibenzo-p-dioxin.

16 the cellular response to the toxic compound 2,3,7,8,-tetrachlorodibenzo-p-dioxin.

17 hrene, fluoranthene, pyrene, benzo(a)pyrene, 2,3,7,8-tetrachlorodibenzo-p-dioxin, 1,2,3,4,6,7,8-hepta

18 OX-2 promoter activity was also increased by 2,3,7,8-tetrachlorodibenzo-p-dioxin, an AhR activator, t

19 AHR ligands (i.e. 2,3,7,8-tetrachlorodibenzo-p-dioxin and alpha-naphthofla

20 hepatocytes in response to AhR activation by 2,3,7,8-tetrachlorodibenzo-p-dioxin and benzo[a]pyrene.

21 ntly identified and shown to be inducible by 2,3,7,8-tetrachlorodibenzo-p-dioxin and hypoxia.

22 and is highly inducible in various organs by 2,3,7,8-tetrachlorodibenzo-p-dioxin and related compound

23 mediates the toxic and biological effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin and related compound

24 Environmental AHR ligands 2,3,7,8-tetrachlorodibenzo[p]dioxin and benzo[a]pyrene m

25 mpared to widespread AHR2-2 in binding TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) and in driving expr

26 logy, such as the toxicity of molecules like 2,3,7,8-tetrachlorodibenzo-p-dioxin as well as regulatio

27 ity of these derivatives to inhibit agonist (2,3,7,8-tetrachlorodibenzo-p-dioxin) binding, nuclear tr

28 ar for each PAH and for the specific agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin but were absent in A

29 nists or presence of the prototypical ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin can affect G1 phase

30 iologically persistent AhR agonists, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin, cause severe toxic

31 on of the aryl hydrocarbon receptor (AHR) by 2,3,7,8-tetrachlorodibenzo-p-dioxin causes altered gene

32 urvey data to assess sex as a determinant of 2,3,7,8-tetrachlorodibenzo-p-dioxin concentration and wi

33 that fires explain 1-10% of the PCDD (5% of 2,3,7,8- tetrachlorodibenzo-p-dioxin) concentrations in

34 d that similar to the established AhR ligand 2,3,7,8,-tetrachlorodibenzo-p-dioxin, curcumin inclusion

35 d to a natural AHR target gene promoter in a 2,3,7,8-tetrachlorodibenzo-p-dioxin -dependent manner.

36 recruited to the CYP1A1 enhancer in a TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin)-dependent fashion i

37 A nongenotoxic AhR ligand (2,3,7,8-tetrachlorodibenzo-p-dioxin) did not elicit grow

38 hors studied immune response and exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin) among veter

39 toxicological response to compounds such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin) and the dev

40 arbon receptor (AHR) plays a central role in 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin) hepatotoxic

41 We studied cancer prevalence and exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin) in veterans

42 ls in epithelial tissues and is inducible by 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin) via the ary

43 toxic responses associated with exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin), and vascul

44 response to environmental pollutants such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin), in the ada

45 s was used to isolate cDNAs corresponding to 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin)-inducible g

46 in developing mice exposed to the pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin).

47 in the toxic events that follow exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin).

48 at mediates the toxicology and teratology of 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin).

49 drocarbons (PAH) and the environmental toxin 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin).

50 The pollutant, 2,3,7,8-tetrachlorodibenzo-p-dioxin ("dioxin"), has been

51 The environmental toxin TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin, dioxin) produces di

52 exes could be detected in cells treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin during hypoxia and n

53 Addition of an AHR antagonist reversed 2,3,7,8-tetrachlorodibenzo-p-dioxin-elicited suppression

54 In contrast, the potent AhR agonist 2,3,7,8-Tetrachlorodibenzo-p-dioxin had no effect on TGF

55 including 7,12-dimethylbenz[a]anthracene and 2,3,7,8-tetrachlorodibenzo[p]dioxin, have been shown to

56 In vitro transformation of the AhR with 2,3,7,8-tetrachlorodibenzo-p-dioxin in cytosol leads to

57 Both forskolin and 2,3,7,8-tetrachlorodibenzo-p-dioxin increased COX-2 mRNA

58 2,3,7,8-Tetrachlorodibenzo-p-dioxin induced cytochrome P

59 AHR activation by its ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin induced functional T

60 (nls) mice were found to be resistant to all 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced toxic respon

61 The environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin induces the microsom

62 Dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin) induces cleft palat

63 These results provide a mechanism by which 2,3,7,8-tetrachlorodibenzo-p-dioxin is able to disrupt e

64 and environmental contaminants like dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin) leads to many adver

65 Seven of these nineteen genes exhibited 2,3,7,8-tetrachlorodibenzo-p-dioxin-mediated regulation,

66 tivation of the aryl hydrocarbon receptor by 2,3,7,8-tetrachlorodibenzo-p-dioxin on long-term self-re

67 Although activation of the AhR by 2,3,7,8-tetrachlorodibenzo-p-dioxin or certain polycycli

68 We delineate a mechanism by which dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin or TCDD)-mediated fo

69 sponse to activation by the canonical ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin resulted in concomit

70 Treatment of these cells with 2,3,7,8-tetrachlorodibenzo-p-dioxin results in a 20-fold

71 Moreover, P450 induction by 2,3,7,8-tetrachlorodibenzo-p-dioxin significantly enhanc

72 t AHR activation by the high-affinity ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin significantly suppre

73 te responses to environmental toxins such as 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD).

74 otent aryl hydrocarbon receptor (AhR) ligand 2,3, 7,8-tetrachlorodibenzo-p-dioxin (TCDD) induced a ap

75 obases of 5'-flanking region, was induced by 2,3, 7,8-tetrachlorodibenzo-p-dioxin (TCDD; 10.0 +/- 3.0

76 These proteins bind 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD) and are able

77 activated transcription factor through which 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD) and related

78 Based on their ability to 1) compete with 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD) for binding

79 Treatment of MCF-7 or Hepa 1c1c7 cells with 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD) resulted in

80 Whereas 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD), a potent ag

81 on of the aryl hydrocarbon receptor (AhR) by 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD), a potent ag

82 n LA2 were extremely low and unresponsive to 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD), basal CYP1B

83 onsistent with this difference, little or no 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible P4

84 to the PAH dimethylbenzanthracene (DMBA) or 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD).

85 in response to the environmental contaminant 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD).

86 als, including the environmental contaminant 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin).

87 Simultaneous treatment of these cells with 2,3,7,8, -tetrachlorodibenzo-p-dioxin (TCDD) and phorbol

88 terine leiomyoma associated with exposure to 2,3,7,8,-tetrachlorodibenzo-p-dioxin (TCDD) for women wh

89 immunosuppressive environmental contaminant 2,3,7,8,-tetrachlorodibenzo-p-dioxin (TCDD) has been sho

90 The environmental pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD = dioxin) has

91 tor soot, a common PCB oil standard and pure 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (normalized a

92 bution of PBDD/Fs was estimated at 162 ng/kg 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (range: 15-67

93 with either 1 nM E2 (target) or E2 plus 1 nM 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (reference) o

94 In animal studies, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) alters glucos

95 analyzed how AhR activation by the pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) alters the in

96 th comparable enhancement being observed for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and also micr

97 Cotreatment of hepa1c1c7 cells with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and Erk kinas

98 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and other ary

99 ure reconstructions and risk assessments for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and other dio

100 ed transcription factor that is activated by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and other rel

101 The effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related c

102 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and related c

103 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and related c

104 otein, mediates most of the toxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related e

105 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and related h

106 an cytochrome P450 cDNA that is inducible by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and represent

107 esponse relationship between serum levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and the occur

108 arbons such as polychlorinated biphenyls and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) are extremely

109 Although the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) are mediated

110 d high benzo[a]pyrene (B[a]P) binding but no 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) binding activ

111 s is constitutively expressed and induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) but also, to

112 atment with a persistent AhR agonist such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) can disrupt G

113 The aryl hydrocarbon receptor (AhR) agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) can disrupt t

114 ch halogenated aromatic hydrocarbons such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) cause altered

115 The environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes a wide

116 that treatment of mice with the AhR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) compromises t

117 zebrafish (Danio rerio) as a model to study 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) developmental

118 AHR hyperactivation by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) during zebraf

119 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) exerts its to

120 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) exhibits anti

121 Because of recent investigations linking 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure in h

122 COS-7 cells expressing zfARNT2b and zfAHR2, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure lead

123 zed for conveying the deleterious effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure.

124 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) impairs crani

125 P450 (CYP) 1A1 mRNA caused by the AHR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in a concentr

126 in regeneration is specifically inhibited by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in adult zebr

127 expressed constitutively and is inducible by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the human

128 ore, we tested whether the potent AHR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induced Cbr1

129 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) induced the 5

130 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) induces nonob

131 We have recently reported that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) inhibits epid

132 at the smoke toxins benzo(a)pyrene (BaP) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) interact with

133 ancer (Lyon, France) recently concluded that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a human ca

134 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a multispe

135 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a persiste

136 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a persiste

137 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a ubiquito

138 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a widespre

139 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a widespre

140 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is an environ

141 ges in gene expression following exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is based upon

142 receptor, for which the environmental toxin 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is the most p

143 ronmental contaminant and potent AHR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) leads to a si

144 Although the toxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on T cells in

145 ed the effect of the prototypical AhR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the expres

146 on of the aryl hydrocarbon receptor (AHR) by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) prevents the

147 cription factor aryl hydrocarbon receptor by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) prevents the

148 new gene that the environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) regulates in

149 on of the aryl hydrocarbon receptor (AhR) by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) resulted in l

150 Exposure to the environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) results in a

151 dition or up to 48 hr before the addition of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) suppressed in

152 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) suppresses ma

153 resistant to proteolysis in the presence of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) than vehicle

154 antially induced by exposure of the cells to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) to levels ran

155 We have demonstrated previously that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) up-regulates

156 Transcription of CYP1A1 is highly induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) via the aryl

157 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) was found to

158 emical substrates (TCB and B[a]P) as well as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) were docked t

159 of androgen-dependent cell proliferation by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) were studied

160 The binding of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) with the aryl

161 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a highly tox

162 One potential stressor is 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a powerful t

163 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a prototypic

164 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a widespread

165 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a widespread

166 ead and persistent organic pollutants, e.g., 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), activate the

167 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), an aryl hydr

168 Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), an environme

169 nds polyaromatic hydrocarbons (PAH), such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), and mediates

170 R), after binding xenobiotic ligands such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), associates w

171 Exposure to dioxins, including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), causes a wid

172 Both rtAHR2alpha and rtAHR2beta bind 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), dimerize wit

173 ediating the toxicity of xenobiotics such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), has more rec

174 e were exposed to a prototypical AhR ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), in utero and

175 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), is primarily

176 on receptor (AhR) by its most potent ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), leads to imm

177 ipid-standardized concentrations of dioxins [2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), polychlorina

178 sitive target for the immunotoxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), possibly by

179 A ligand to the aryl hydrocarbon receptor, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), produced a s

180 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), the most tox

181 ked foods include benzo(a)pyrene [B(a)P] and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), which have b

182 The aromatic hydrocarbon receptor ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), which is not

183 tein similar to the conformational change of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-bound AhR.

184 rocarbon receptor (AhR) in the regulation of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced apopt

185 siRNA for the AhR also decreased 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced CYP1A

186 uman hepatoma cells, DBM inhibited DMBA- and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced enzym

187 xpression of AhR by LPS and the LPS-enhanced 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-mediated indu

188 in mice treated with the potent AhR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

189 riety of environmental pollutants, including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

190 of target genes upon binding ligands such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

191 carbonitrile (PCN) or the Ah receptor ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

192 NT to mediate responses to compounds such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

193 6-fold greater than that achieved with only 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

194 hat mediates most toxic responses induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

195 on in the maximal level of CYP1A1 induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

196 y the aryl hydrocarbon receptor (AhR) ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

197 carbazoles was similar to that observed for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

198 omatic environmental contaminants, including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

199 d in response to ligand binding, typified by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

200 ion-specific differences in its affinity for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

201 tabolizable aryl hydrocarbon receptor ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

202 r 2,3,7,8-tetrachlorodibenzofuran (TCDF) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

203 nd generation of antibodies for detection of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

204 ive target for the toxic effects produced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

205 hat respond to the environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

206 h as the synthetic environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

207 lecular level the antiestrogenic activity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

208 t) protein in culture cell models exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

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

210 ncluding the toxic environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

211 mental pollutants Benzo[a]pyrene (B[a]P) and 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD).

212 those induced by xenobiotic ligands, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

213 anscription induced by the potent carcinogen 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

214 for the Ah receptor by competition with [3H]2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

215 esponse to the exogenous prototypical ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

216 the aryl hydrocarbon receptor (AhR) ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

217 with a panel of activating ligands for AhR [2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)], CAR [6-(4-c

218 The environmental pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin) cause

219 ts of the environmental toxin and carcinogen 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin) inclu

220 nd halogenated aromatic hydrocarbons such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin).

221 nd-activated transcription factor that binds 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin).

222 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD, or dioxin) is

223 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD; dioxin) is a

224 Oxidative stress induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; dioxin) is po

225 Dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin, TCDD) is a carcinog

226 urrent study examined the ability of dioxin (2,3,7,8-tetrachlorodibenzo[p]dioxin, TCDD) to promote ep

227 cts of the environmental contaminant dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin; TCDD).

228 In response to 2,3,7,8-tetrachlorodibenzo-p-dioxin, the AHR.

229 ling pathway was activated during hypoxia by 2,3,7,8-tetrachlorodibenzo-p-dioxin, the induction of P4

230 duction of CYP1A1 enzyme activity by FICZ or 2,3,7,8-tetrachlorodibenzo-p-dioxin, thereby subsequentl

231 ergize with an environmental agonist of AhR (2,3,7,8-tetrachlorodibenzo-p-dioxin) to potentiate AhR t

232 ontained covalent adducts, whereas that from 2,3,7,8-tetrachlorodibenzo-p-dioxin-treated cells did no

233 oplasmic localization, which was reversed by 2,3,7, 8-tetrachlorodibenzo-p-dioxin treatment (TCDD).

234 with unliganded Ah receptor and with hsp90; 2,3,7,8-tetrachlorodibenzo-p-dioxin treatment disrupts t

235 tection limit of the assays for atrazine and 2,3,7,8-tetrachlorodibenzo-p-dioxin was 2.0 x 10(-10) M

236 is than DMBA, whereas the potent AhR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin was inactive.

237 tter understand the mechanism of toxicity of 2,3,7, 8-tetrachlorodibenzo-p-dioxin, we employed an ite

238 d with the aryl hydrocarbon receptor agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin whereas the equivale

239 ffinity for prototypical AHR ligands such as 2,3,7,8-tetrachlorodibenzo-p-dioxin, which has been attr

240 al effects of the environmental contaminant, 2,3,7,8-tetrachlorodibenzo-p-dioxin, which include the t

241 o express CYP1A1 mRNA even when treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin, which induces this