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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 e toxicologic and carcinogenic properties of 2,3,7,8-tetrachlorodibenzo-p-dioxin.
5 the environmental contaminant and AHR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin.
6 atoma cells to the microsomal enzyme inducer 2,3,7,8-tetrachlorodibenzo-p-dioxin.
7 l toxicants such as 3-methylcholanthrene and 2,3,7,8-tetrachlorodibenzo-p-dioxin.
8 ose of the most potent dioxin-like compound, 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 undant skin ceramides were also increased by 2,3,7,8-tetrachlorodibenzo-p-dioxin.
12 m studies using the toxic synthetic chemical 2,3,7,8-tetrachlorodibenzo-p-dioxin.
13 l treatment with IL1beta and the AHR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin.
14 e of increased disease risk from exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin.
15 r that mediates the effects of agonists like 2,3, 7,8-tetrachlorodibenzo-p-dioxin.
16 ponses to environmental contaminants such as 2,3,7, 8-tetrachlorodibenzo-p-dioxin.
17  the cellular response to the toxic compound 2,3,7,8,-tetrachlorodibenzo-p-dioxin.
18 hrene, fluoranthene, pyrene, benzo(a)pyrene, 2,3,7,8-tetrachlorodibenzo-p-dioxin, 1,2,3,4,6,7,8-hepta
19 s the inocula in a secondary experiment with 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TeCDD), 1,2
20 OX-2 promoter activity was also increased by 2,3,7,8-tetrachlorodibenzo-p-dioxin, an AhR activator, t
21                            AHR ligands (i.e. 2,3,7,8-tetrachlorodibenzo-p-dioxin and alpha-naphthofla
22 hepatocytes in response to AhR activation by 2,3,7,8-tetrachlorodibenzo-p-dioxin and benzo[a]pyrene.
23 ntly identified and shown to be inducible by 2,3,7,8-tetrachlorodibenzo-p-dioxin and hypoxia.
24 and is highly inducible in various organs by 2,3,7,8-tetrachlorodibenzo-p-dioxin and related compound
25 mediates the toxic and biological effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin and related compound
26                    Environmental AHR ligands 2,3,7,8-tetrachlorodibenzo[p]dioxin and benzo[a]pyrene m
27 mpared to widespread AHR2-2 in binding TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) and in driving expr
28 nds, including the environmental toxin TCDD, 2,3,7,8-tetrachlorodibenzo-p-dioxin, and naturally occur
29 logy, such as the toxicity of molecules like 2,3,7,8-tetrachlorodibenzo-p-dioxin as well as regulatio
30 ity of these derivatives to inhibit agonist (2,3,7,8-tetrachlorodibenzo-p-dioxin) binding, nuclear tr
31 ar for each PAH and for the specific agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin but were absent in A
32 nists or presence of the prototypical ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin can affect G1 phase
33 iologically persistent AhR agonists, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin, cause severe toxic
34 on of the aryl hydrocarbon receptor (AHR) by 2,3,7,8-tetrachlorodibenzo-p-dioxin causes altered gene
35 urvey data to assess sex as a determinant of 2,3,7,8-tetrachlorodibenzo-p-dioxin concentration and wi
36  that fires explain 1-10% of the PCDD (5% of 2,3,7,8- tetrachlorodibenzo-p-dioxin) concentrations in
37 d that similar to the established AhR ligand 2,3,7,8,-tetrachlorodibenzo-p-dioxin, curcumin inclusion
38 d to a natural AHR target gene promoter in a 2,3,7,8-tetrachlorodibenzo-p-dioxin -dependent manner.
39  recruited to the CYP1A1 enhancer in a TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin)-dependent fashion i
40                   A nongenotoxic AhR ligand (2,3,7,8-tetrachlorodibenzo-p-dioxin) did not elicit grow
41 hors studied immune response and exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin) among veter
42  toxicological response to compounds such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin) and the dev
43 arbon receptor (AHR) plays a central role in 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin) hepatotoxic
44 We studied cancer prevalence and exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin) in veterans
45 ls in epithelial tissues and is inducible by 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin) via the ary
46  toxic responses associated with exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin), and vascul
47 response to environmental pollutants such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin), in the ada
48 s was used to isolate cDNAs corresponding to 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin)-inducible g
49  in developing mice exposed to the pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin).
50  in the toxic events that follow exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin).
51 at mediates the toxicology and teratology of 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin).
52 drocarbons (PAH) and the environmental toxin 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin).
53                               The pollutant, 2,3,7,8-tetrachlorodibenzo-p-dioxin ("dioxin"), has been
54                The environmental toxin TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin, dioxin) produces di
55 exes could be detected in cells treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin during hypoxia and n
56       Addition of an AHR antagonist reversed 2,3,7,8-tetrachlorodibenzo-p-dioxin-elicited suppression
57          In contrast, the potent AhR agonist 2,3,7,8-Tetrachlorodibenzo-p-dioxin had no effect on TGF
58 including 7,12-dimethylbenz[a]anthracene and 2,3,7,8-tetrachlorodibenzo[p]dioxin, have been shown to
59      In vitro transformation of the AhR with 2,3,7,8-tetrachlorodibenzo-p-dioxin in cytosol leads to
60                           Both forskolin and 2,3,7,8-tetrachlorodibenzo-p-dioxin increased COX-2 mRNA
61 man epidermal keratinocytes, the AHR ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin, increased RNA level
62                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin induced cytochrome P
63                 AHR activation by its ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin induced functional T
64 (nls) mice were found to be resistant to all 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced toxic respon
65                The environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin induces the microsom
66                                      Dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin) induces cleft palat
67   These results provide a mechanism by which 2,3,7,8-tetrachlorodibenzo-p-dioxin is able to disrupt e
68  and environmental contaminants like dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin) leads to many adver
69      Seven of these nineteen genes exhibited 2,3,7,8-tetrachlorodibenzo-p-dioxin-mediated regulation,
70    The AHR antagonist, GNF351, inhibited the 2,3,7,8-tetrachlorodibenzo-p-dioxin-mediated RNA and tra
71 tivation of the aryl hydrocarbon receptor by 2,3,7,8-tetrachlorodibenzo-p-dioxin on long-term self-re
72            Although activation of the AhR by 2,3,7,8-tetrachlorodibenzo-p-dioxin or certain polycycli
73    We delineate a mechanism by which dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin or TCDD)-mediated fo
74 sponse to activation by the canonical ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin resulted in concomit
75                Treatment of these cells with 2,3,7,8-tetrachlorodibenzo-p-dioxin results in a 20-fold
76                  Moreover, P450 induction by 2,3,7,8-tetrachlorodibenzo-p-dioxin significantly enhanc
77 t AHR activation by the high-affinity ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin significantly suppre
78 te responses to environmental toxins such as 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD).
79 otent aryl hydrocarbon receptor (AhR) ligand 2,3, 7,8-tetrachlorodibenzo-p-dioxin (TCDD) induced a ap
80 obases of 5'-flanking region, was induced by 2,3, 7,8-tetrachlorodibenzo-p-dioxin (TCDD; 10.0 +/- 3.0
81                          These proteins bind 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD) and are able
82 activated transcription factor through which 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD) and related
83    Based on their ability to 1) compete with 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD) for binding
84  Treatment of MCF-7 or Hepa 1c1c7 cells with 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD) resulted in
85                                      Whereas 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD), a potent ag
86 on of the aryl hydrocarbon receptor (AhR) by 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD), a potent ag
87 n LA2 were extremely low and unresponsive to 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD), basal CYP1B
88 onsistent with this difference, little or no 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible P4
89  to the PAH dimethylbenzanthracene (DMBA) or 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD).
90 in response to the environmental contaminant 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD).
91 als, including the environmental contaminant 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin).
92   Simultaneous treatment of these cells with 2,3,7,8, -tetrachlorodibenzo-p-dioxin (TCDD) and phorbol
93 terine leiomyoma associated with exposure to 2,3,7,8,-tetrachlorodibenzo-p-dioxin (TCDD) for women wh
94  immunosuppressive environmental contaminant 2,3,7,8,-tetrachlorodibenzo-p-dioxin (TCDD) has been sho
95                  The environmental pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD = dioxin) has
96 tor soot, a common PCB oil standard and pure 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (normalized a
97 bution of PBDD/Fs was estimated at 162 ng/kg 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (range: 15-67
98 with either 1 nM E2 (target) or E2 plus 1 nM 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (reference) o
99                           In animal studies, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) alters glucos
100 analyzed how AhR activation by the pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) alters the in
101 th comparable enhancement being observed for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and also micr
102          Cotreatment of hepa1c1c7 cells with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and Erk kinas
103                                              2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and other ary
104 ure reconstructions and risk assessments for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and other dio
105 ription factor that mediates the toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and other pla
106 ed transcription factor that is activated by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and other rel
107                               The effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related c
108                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and related c
109                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and related c
110 on factor known for mediating the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related c
111 otein, mediates most of the toxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related e
112                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and related h
113 an cytochrome P450 cDNA that is inducible by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and represent
114 esponse relationship between serum levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and the occur
115 tween this SNP and AHR expression after both 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and ultraviol
116 arbons such as polychlorinated biphenyls and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) are extremely
117                      Although the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) are mediated
118 d high benzo[a]pyrene (B[a]P) binding but no 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) binding activ
119 s is constitutively expressed and induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) but also, to
120 atment with a persistent AhR agonist such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) can disrupt G
121  The aryl hydrocarbon receptor (AhR) agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) can disrupt t
122 ch halogenated aromatic hydrocarbons such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) cause altered
123                The environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes a wide
124                The environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes hepati
125  that treatment of mice with the AhR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) compromises t
126  zebrafish (Danio rerio) as a model to study 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) developmental
127                       AHR hyperactivation by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) during zebraf
128 ity in male C57BL/6 mice orally gavaged with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) every 4 days
129                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) exerts its to
130                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) exhibits anti
131     Because of recent investigations linking 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure in h
132  COS-7 cells expressing zfARNT2b and zfAHR2, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure lead
133                   We evaluated the impact of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure, a u
134 zed for conveying the deleterious effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure.
135                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) impairs crani
136 P450 (CYP) 1A1 mRNA caused by the AHR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in a concentr
137 in regeneration is specifically inhibited by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in adult zebr
138 expressed constitutively and is inducible by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the human
139 ore, we tested whether the potent AHR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induced Cbr1
140                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) induced the 5
141                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) induces nonob
142               We have recently reported that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) inhibits epid
143 at the smoke toxins benzo(a)pyrene (BaP) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) interact with
144 ancer (Lyon, France) recently concluded that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a human ca
145                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a multispe
146                                              2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a persiste
147                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a persiste
148                                              2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a persiste
149                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a persiste
150                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a ubiquito
151                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a widespre
152                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a widespre
153                                              2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is an environ
154                                              2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is associated
155 ges in gene expression following exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is based upon
156  receptor, for which the environmental toxin 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is the most p
157 ronmental contaminant and potent AHR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) leads to a si
158                Although the toxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on T cells in
159 ed the effect of the prototypical AhR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the expres
160 on of the aryl hydrocarbon receptor (AHR) by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) prevents the
161 cription factor aryl hydrocarbon receptor by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) prevents the
162  new gene that the environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) regulates in
163 on of the aryl hydrocarbon receptor (AhR) by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) resulted in l
164    Exposure to the environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) results in a
165 dition or up to 48 hr before the addition of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) suppressed in
166                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) suppresses ma
167  resistant to proteolysis in the presence of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) than vehicle
168 ponse to xenobiotics, including prototypical 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) through the a
169 antially induced by exposure of the cells to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) to levels ran
170         We have demonstrated previously that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) up-regulates
171 Transcription of CYP1A1 is highly induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) via the aryl
172                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) was found to
173 emical substrates (TCB and B[a]P) as well as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) were docked t
174  of androgen-dependent cell proliferation by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) were studied
175                               The binding of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) with the aryl
176 to investigate how developmental exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a high-affin
177                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a highly tox
178 posure to environmentally relevant levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a model comp
179                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a persistent
180                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a persistent
181  by gene ablation or by in utero exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a potent AHR
182 ryl hydrocarbon receptor (AhR) activation by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a potent lig
183                    One potential stressor is 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a powerful t
184                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a prototypic
185                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a widespread
186                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a widespread
187 ead and persistent organic pollutants, e.g., 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), activate the
188                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), an aryl hydr
189                                 The compound 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), an environme
190                                  Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), an environme
191                  The toxic manifestations of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), an environme
192 nds polyaromatic hydrocarbons (PAH), such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), and mediates
193 R), after binding xenobiotic ligands such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), associates w
194 DDs, 2,3-dichlorodibenzo-p-dioxin (BCDD) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), based on the
195 says showed that both gmAhr proteins bind to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), but stronger
196               Exposure to dioxins, including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), causes a wid
197         Both rtAHR2alpha and rtAHR2beta bind 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), dimerize wit
198                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), for which th
199            In rodents, the prototypical DLC, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), has been sho
200 ediating the toxicity of xenobiotics such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), has more rec
201 e were exposed to a prototypical AhR ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), in utero and
202 ical aryl hydrocarbon receptor (AHR) ligand, 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), induces CYP1
203                                              2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), is primarily
204 on receptor (AhR) by its most potent ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), leads to imm
205 ipid-standardized concentrations of dioxins [2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), polychlorina
206 sitive target for the immunotoxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), possibly by
207   A ligand to the aryl hydrocarbon receptor, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), produced a s
208                                              2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), the most tox
209 ked foods include benzo(a)pyrene [B(a)P] and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), which have b
210     The aromatic hydrocarbon receptor ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), which is not
211 tein similar to the conformational change of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-bound AhR.
212 rocarbon receptor (AhR) in the regulation of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced apopt
213             siRNA for the AhR also decreased 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced CYP1A
214 uman hepatoma cells, DBM inhibited DMBA- and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced enzym
215 xpression of AhR by LPS and the LPS-enhanced 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-mediated indu
216  the aryl hydrocarbon receptor (AhR) ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
217  in mice treated with the potent AhR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
218 riety of environmental pollutants, including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
219 of target genes upon binding ligands such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
220 carbonitrile (PCN) or the Ah receptor ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
221 NT to mediate responses to compounds such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
222  6-fold greater than that achieved with only 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
223 hat mediates most toxic responses induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
224 nist StemReginin-1 (SR-1) or the AHR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
225 on in the maximal level of CYP1A1 induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
226 y the aryl hydrocarbon receptor (AhR) ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
227 omatic environmental contaminants, including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
228 d in response to ligand binding, typified by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
229 tabolizable aryl hydrocarbon receptor ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
230 esponse to the exogenous prototypical ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
231 r 2,3,7,8-tetrachlorodibenzofuran (TCDF) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
232 nd generation of antibodies for detection of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
233 ive target for the toxic effects produced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
234 hat respond to the environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
235 h as the synthetic environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
236 lecular level the antiestrogenic activity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
237 t) protein in culture cell models exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
238  carbazoles was similar to that observed for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
239 ion-specific differences in its affinity for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
240 e AHR is an environmental contaminant called 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
241 ncluding the toxic environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
242 mental pollutants Benzo[a]pyrene (B[a]P) and 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD).
243 those induced by xenobiotic ligands, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
244 anscription induced by the potent carcinogen 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
245  for the Ah receptor by competition with [3H]2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).
246  with a panel of activating ligands for AhR [2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)], CAR [6-(4-c
247                  The environmental pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin) cause
248 ts of the environmental toxin and carcinogen 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin) inclu
249 nd halogenated aromatic hydrocarbons such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin).
250 nd-activated transcription factor that binds 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin).
251                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD, or dioxin) is
252                                              2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD; dioxin) is a
253                  Oxidative stress induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; dioxin) is po
254                                      Dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin, TCDD) is a carcinog
255 urrent study examined the ability of dioxin (2,3,7,8-tetrachlorodibenzo[p]dioxin, TCDD) to promote ep
256 cts of the environmental contaminant dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin; TCDD).
257                               In response to 2,3,7,8-tetrachlorodibenzo-p-dioxin, the AHR.
258 ling pathway was activated during hypoxia by 2,3,7,8-tetrachlorodibenzo-p-dioxin, the induction of P4
259 compared to the rank order of sensitivity to 2,3,7,8-tetrachlorodibenzo[p]dioxin, the prototypical Ah
260 duction of CYP1A1 enzyme activity by FICZ or 2,3,7,8-tetrachlorodibenzo-p-dioxin, thereby subsequentl
261 ergize with an environmental agonist of AhR (2,3,7,8-tetrachlorodibenzo-p-dioxin) to potentiate AhR t
262 ontained covalent adducts, whereas that from 2,3,7,8-tetrachlorodibenzo-p-dioxin-treated cells did no
263 oplasmic localization, which was reversed by 2,3,7, 8-tetrachlorodibenzo-p-dioxin treatment (TCDD).
264  with unliganded Ah receptor and with hsp90; 2,3,7,8-tetrachlorodibenzo-p-dioxin treatment disrupts t
265 tection limit of the assays for atrazine and 2,3,7,8-tetrachlorodibenzo-p-dioxin was 2.0 x 10(-10) M
266 is than DMBA, whereas the potent AhR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin was inactive.
267 tter understand the mechanism of toxicity of 2,3,7, 8-tetrachlorodibenzo-p-dioxin, we employed an ite
268 g the high-affinity and AHR-specific agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin, we show that AHR ac
269 d with the aryl hydrocarbon receptor agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin whereas the equivale
270 ffinity for prototypical AHR ligands such as 2,3,7,8-tetrachlorodibenzo-p-dioxin, which has been attr
271 al effects of the environmental contaminant, 2,3,7,8-tetrachlorodibenzo-p-dioxin, which include the t
272 o express CYP1A1 mRNA even when treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin, which induces this

 
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