Transcriptional roles of AhR in expression of biological effects induced by endocrine disruptors

Verfasser / Beitragende:
[Yoshiaki Fujii-Kuriyama, J. Mimura]
Ort, Verlag, Jahr:
2003
Enthalten in:
Pure and Applied Chemistry, 75/11-12(2003-01-01), 1819-1826
Format:
Artikel (online)
ID: 378861697
LEADER caa a22 4500
001 378861697
003 CHVBK
005 20180305123348.0
007 cr unu---uuuuu
008 161128e20030101xx s 000 0 eng
024 7 0 |a 10.1351/pac200375111819  |2 doi 
035 |a (NATIONALLICENCE)gruyter-10.1351/pac200375111819 
245 0 0 |a Transcriptional roles of AhR in expression of biological effects induced by endocrine disruptors  |h [Elektronische Daten]  |c [Yoshiaki Fujii-Kuriyama, J. Mimura] 
520 3 |a 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), one of most toxic man-made chemicals, binds arylhydrocarbon receptor (AhR or dioxin receptor), whose endogenous ligand remains unknown, with an extremely high affinity and expresses pleiotropic biological effects. From analysis of the primary structures, AhR belongs to a distinct group of a super-gene family from that of nuclear receptors. PCB, 3-methylcholanthrene, and benzo(a)pyrene are also ligands to the AhR, and these polycyclic aromatic chemicals are considered to display pleiotropic biological effects such as induction of a variety of drug-metabolizing enzymes, teratogenesis, tumor promotion, immunodeficiency due to thymic involution, and liver damage. Generation of the AhR-deficient mice by gene knock-out technology revealed that these biological effects described are mediated by AhR, because AhR(-/-) mice lost susceptibility to these effects by TCDD and benzo(a) pyrene. It has recently been revealed that AhR is also involved in reproduction of female mice. Although the detailed mechanisms of involvement of AhR in exerting these effects are not always clarified, AhR is generally considered to function as a transcription factor, which activates the expression of genes by binding directly the XRE sequence in their promoter in a heterodimer form with Arnt. From analysis of DNA transfection and GST pull-down assays, it is revealed that AhR and Arnt interact with various coactivators such as RIP140, SRC-1/NcoA, and CBP/p300 to transmit their transactivation activity to general transcription factors (GTFs). AhR has also been shown to interact with various regulatory factors including Rb, NF-κB, and SP1, resulting in mutual inhibition or synergistic enhancement of their activities depending on the mode of localization of their cognate binding sequences in the target genes. Agonistic and antagonistic properties of various ligands to AhR also are discussed. 
540 |a © 2013 Walter de Gruyter GmbH, Berlin/Boston 
700 1 |a Fujii-Kuriyama  |D Yoshiaki  |u Center for Tsukuba Advanced Research Alliance, University of Tsukuba, Tennoudai, 1-1-1, Tsukuba, Ibaraki, 305-8577, Japan  |4 aut 
700 1 |a Mimura  |D J.  |u Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation  |4 aut 
773 0 |t Pure and Applied Chemistry  |d De Gruyter  |g 75/11-12(2003-01-01), 1819-1826  |x 0033-4545  |q 75:11-12<1819  |1 2003  |2 75  |o pac 
856 4 0 |u https://doi.org/10.1351/pac200375111819  |q text/html  |z Onlinezugriff via DOI 
908 |D 1  |a research article  |2 jats 
950 |B NATIONALLICENCE  |P 856  |E 40  |u https://doi.org/10.1351/pac200375111819  |q text/html  |z Onlinezugriff via DOI 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Fujii-Kuriyama  |D Yoshiaki  |u Center for Tsukuba Advanced Research Alliance, University of Tsukuba, Tennoudai, 1-1-1, Tsukuba, Ibaraki, 305-8577, Japan  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Mimura  |D J.  |u Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation  |4 aut 
950 |B NATIONALLICENCE  |P 773  |E 0-  |t Pure and Applied Chemistry  |d De Gruyter  |g 75/11-12(2003-01-01), 1819-1826  |x 0033-4545  |q 75:11-12<1819  |1 2003  |2 75  |o pac 
900 7 |b CC0  |u http://creativecommons.org/publicdomain/zero/1.0  |2 nationallicence 
898 |a BK010053  |b XK010053  |c XK010000 
949 |B NATIONALLICENCE  |F NATIONALLICENCE  |b NL-gruyter