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Drug-Target Interaction

Drug

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PubChem ID:15625
Structure:
Synonyms:
1746-01-6
2,3,7,8-:tetrachlorodibenzo-p-dioxin
2,3,7,8-Czterochlorodwubenzo-p-dwuoksyny
2,3,7,8-Czterochlorodwubenzo-p-dwuoksyny [Polish]
2,3,7,8-T4CDD
2,3,7,8-TCDD
2,3,7,8-Tetra polychlorinated dibenzo-p-dioxin
2,3,7,8-Tetrachloro(b,e)dibenzodioxin
2,3,7,8-Tetrachloro(b,f)dibenzodioxin
2,3,7,8-Tetrachloro-dibenzo[b,e][1,4]dioxin
2,3,7,8-Tetrachlorodibenzo(b,e)(1,4)dioxin
2,3,7,8-Tetrachlorodibenzo-1,4-dioxin
2,3,7,8-Tetrachlorodibenzo-p-dioxin
2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN (SEE ALSO TRANSGENIC MODEL EVALUATION
2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN (SEE ALSO TRANSGENIC MODEL EVALUATION (2,3,7,8-TETRACHLORODIBENZODIOXIN))
2,3,7,8-Tetrachlorodibenzo-p-dioxin [Dioxin and dioxin-like compounds]
2,3,7,8-Tetrachlorodibenzodioxin
2,3,7,8-tetrachlorodibenzodioxine
2,3,7,8-Tetrachlorodibenzo[b,e][1,4]dioxin
2,3,7,8-tetrachlorooxanthrene
5-19-02-00041 (Beilstein Handbook Reference)
56795-67-6
AC1L26AF
AIDS-105033
AIDS105033
BRN 0271116
C07557
CCRIS 576
CHEBI:28119
CHEMBL30327
D013749
Dibenzo(b,e)(1,4)dioxin, 2,3,7,8-tetrachloro-
dibenzo-dioxin, 2,3,7,8-tetrachlorinated
Dibenzo-p-dioxin, 2,3,7,8-tetrachloro-
Dioksyny
Dioksyny [Polish]
Dioxin
Dioxin (herbicide contaminant)
Dioxin mixture
Dioxine
EINECS 217-122-7
HSDB 4151
LS-938
NCI-C03714
PCDD 48
TCDB D
TCDBD
TCDD
TEF TRANSGENICS (TCDD)
Tetrachlorodibenzo-1,4-dioxin
Tetrachlorodibenzo-p-dioxin
Tetrachlorodibenzodioxin
Tetradioxin
TOXIC EQUIVALENCY FACTOR EVALUATION (TCDD) (SEE ALSO TCDD & TRANSGENIC MODEL EVALUATION)
TRANSGENIC MODEL EVALUATION (2,3,7,8-TETRACHLORODIBENZODIOXIN)
[3H]-TCDD

Target

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Uniprot ID:RARA_HUMAN
Synonyms:
Nuclear receptor subfamily 1 group B member 1
RAR-alpha
Retinoic acid receptor alpha
EC-Numbers:-
Organism:Homo sapiens
Human
PDB IDs:1DKF 1DSZ
Structure:
1DSZ

Binding Affinities:

Ki: Kd:Ic 50:Ec50/Ic50:
----

References:

16480812
The aryl hydrocarbon receptor activates the retinoic acid receptoralpha through SMRT antagonism.. Magdalena Widerak; Christelle Ghoneim; Marie-France Dumontier; Monique Quesne; Marie Therese Corvol; Jean-Francois Savouret (2006) Biochimie display abstract
Aryl hydrocarbon receptor (AhR) ligands such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) or benzo(a)pyrene interfere with hormonal regulatory pathways, leading to endocrine disruption. Notably, the activated AhR exerts complex effects on estrogens and retinoids at both levels of their metabolism and regulation of cognate genes. Our current investigation of these AhR effects revealed the TCDD-dependent activation of a subset of retinoid-dependent genes (tissue-transglutaminase, IGF binding protein-3, AhR) in MCF-7 breast cancer cells. A collection of in vitro hormone-dependent reporter gene models showed that AhR activation by TCDD stimulated transactivation by several class I heteromeric receptors (retinoic and thyroid hormone receptors) while it antagonized homodimeric nuclear receptors (estrogen and progesterone receptors, ER and PR). TCDD exerted a dose-dependent effect on a retinoic acid-dependent reporter gene expressed in MCF-7 cells. AhR was shown to be involved in a mutual antagonism with RARalpha corepressor SMRT (silencing mediator of retinoid and thyroid receptors). This, and the documented physical interaction between AhR and SMRT suggested that SMRT sequestration by AhR might activate RARalpha in the absence of ligand. Immunocytochemical studies of AhR and SMRT strongly suggested they colocalized in nuclear bodies during this sequestration. Concurring with this interpretation, we observed an interaction in vitro between AhR and the PML protein, the core component of nuclear bodies. This ability of AhR to elicit spurious activation of retinoid receptors expands the scope of AhR ligands influence beyond ER antagonism and specific Dioxin-responsive genes. Unknown AhR endogenous ligands may also elicit gene transactivation by class I receptors, while being inactive on classic xenobiotic-responsive genes.