期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 280, 期 22, 页码 21607-21611出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.C500090200
关键词
-
资金
- NIEHS NIH HHS [ES04869] Funding Source: Medline
The aryl hydrocarbon receptor (AHR) and the aryl hydrocarbon receptor nuclear translocator (ARNT) form a heterodimeric transcription factor upon binding a wide variety of environmental pollutants, including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). AHR target gene activation can be repressed by estrogen and estrogen-like compounds. In this study, we demonstrate that a significant component of TCDD-inducible Cyp1a1 transcription is the result of recruitment of estrogen receptor (ER)-alpha by AHR/ARNT as a transcriptional corepressor. Both AHR and ARNT were capable of interacting directly with ER alpha, as ascertained by glutathione S-transferase pull-down. 17 beta-estradiol repressed TCDD-activated Cyp1a1 and Cyp1b1 gene transcription in MCF-7 cells in the presence of cycloheximide, as determined by reverse transcription/real-time PCR. Furthermore, chromatin immunoprecipitation (ChIP) assays have shown that ER alpha is present at the Cyp1a1 enhancer only after co-treatment with E2 and TCDD, in MCF-7 cells. Sequential two-step ChIP assays were performed which demonstrate that AHR and ER alpha are present together at the same time on the Cyp1a1 enhancer during transrepression. Taken together these data support a role for ER-mediated transrepression of AHR-dependent gene regulation.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据