学科主题临床医学
Dismissal of RNA Polymerase II Underlies a Large Ligand-Induced Enhancer Decommissioning Program
Tan, Yuliang1; Jin, Chunyu1; Ma, Wubin1; Hu, Yiren1; Tanasa, Bogdan2; Oh, Soohwan1,3; Gamliel, Amir1; Ma, Qi1,4; Yao, Lu1,5; Zhang, Jie1; Ohgi, Kenny1; Liu, Wen1,6; Aggarwal, Aneel K.7; Rosenfeld, Michael G.1
通讯作者Rosenfeld, Michael G.(1)
刊名MOLECULAR CELL
2018-08-16
DOI10.1016/j.molcel.2018.07.039
71期:4页:526-+
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology ; Cell Biology
研究领域[WOS]Biochemistry & Molecular Biology ; Cell Biology
关键词[WOS]PLURIPOTENT STEM-CELLS ; DNA-BINDING DOMAIN ; ESTROGEN-RECEPTOR ; GENE-EXPRESSION ; BREAST-CANCER ; HUMAN GENOME ; TRANSCRIPTIONAL ACTIVATION ; CHROMATIN INTERACTIONS ; READ ALIGNMENT ; HISTONE H3
英文摘要

Nuclear receptors induce both transcriptional activation and repression programs responsible for development, homeostasis, and disease. Here, we report a previously overlooked enhancer decommissioning strategy underlying a large estrogen receptor alpha (ER alpha)-dependent transcriptional repression program. The unexpected signature for this E-2-induced program resides in indirect recruitment of ER alpha to a large cohort of pioneer factor basally active FOXA1-bound enhancers that lack cognate ER alpha DNA-binding elements. Surprisingly, these basally active estrogen-repressed (BAER) enhancers are decommissioned by ER alpha-dependent recruitment of the histone demethylase KDM2A, functioning independently of its demethylase activity. Rather, KDM2A tethers the E3 ubiquitin-protein ligase NEDD4 to ubiquitylate/dismiss Pol II to abrogate eRNA transcription, with consequent target gene downregulation. Thus, our data reveal that Pol II ubiquitylation/dismissal may serve as a potentially broad strategy utilized by indirectly bound nuclear receptors to abrogate large programs of pioneer factor-mediated, eRNA-producing enhancers.

语种英语
WOS记录号WOS:000441745600007
通讯作者邮箱mrosenfeld@ucsd.edu
ISSN1097-2765
引用统计
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/142891
专题北京大学临床肿瘤学院_乳腺癌预防治疗中心
作者单位1.Univ Calif San Diego, Howard Hughes Med Inst, Dept Med, 9500 Gilman Dr, La Jolla, CA 92093 USA;
2.Univ Calif San Diego, Biol Sci Grad Program, La Jolla, CA 92093 USA;
3.Univ Calif San Diego, Bioinformat & Syst Biol Grad Program, La Jolla, CA 92093 USA;
4.Peking Univ, Canc Hosp & Inst, Breast Ctr, Minist Educ,Key Lab Carcinogenesis & Translat Res, Beijing 100142, Peoples R China;
5.Xiamen Univ, Fujian Prov Key Lab Innovat Drug Target Res, Sch Pharmaceut Sci, Xiangan South Rd, Xiamen 361102, Fujian, Peoples R China;
6.Mt Sinai Sch Med, Dept Struct & Chem Biol, Box 1677,1425 Madison Ave, New York, NY 10029 USA;
7.Stanford Univ, Sch Med, 265 Campus Dr,LLSCR Bldg, Stanford, CA 94305 USA
推荐引用方式
GB/T 7714
Tan, Yuliang,Jin, Chunyu,Ma, Wubin,et al. Dismissal of RNA Polymerase II Underlies a Large Ligand-Induced Enhancer Decommissioning Program[J]. MOLECULAR CELL,2018,71(4):526-+.
APA Tan, Yuliang.,Jin, Chunyu.,Ma, Wubin.,Hu, Yiren.,Tanasa, Bogdan.,...&Rosenfeld, Michael G..(2018).Dismissal of RNA Polymerase II Underlies a Large Ligand-Induced Enhancer Decommissioning Program.MOLECULAR CELL,71(4),526-+.
MLA Tan, Yuliang,et al."Dismissal of RNA Polymerase II Underlies a Large Ligand-Induced Enhancer Decommissioning Program".MOLECULAR CELL 71.4(2018):526-+.
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