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题名: ELL Inhibits E2F1 Transcriptional Activity by Enhancing E2F1 Deacetylation via Recruitment of Histone Deacetylase 1
作者: Zhang, Wei1; Ji, Wei1; Liu, Xing1; Ouyang, Gang1; Xiao, Wuhan1
通讯作者: Xiao, WH (reprint author), Chinese Acad Sci, Inst Hydrobiol, Key Lab Aquat Biodivers & Conservat, Wuhan, Peoples R China.
关键词: RNA-POLYMERASE-II ; ELONGATION-FACTOR ELL ; MIXED-LINEAGE LEUKEMIA ; DNA-DAMAGE ; COMPLEX SEC ; CELL-DEATH ; MLL-ELL ; PROTEIN ; GENE ; TRANSACTIVATION
刊名: MOLECULAR AND CELLULAR BIOLOGY
发表日期: 2014-02-01
DOI: 10.1128/MCB.00878-13
卷: 34, 期:4, 页:765-775
收录类别: SCI
文章类型: Article
部门归属: [Zhang, Wei; Ji, Wei; Liu, Xing; Ouyang, Gang; Xiao, Wuhan] Chinese Acad Sci, Inst Hydrobiol, Key Lab Aquat Biodivers & Conservat, Wuhan, Peoples R China
WOS标题词: Science & Technology ; Life Sciences & Biomedicine
资助者: 973 grant [2010CB126306]; CAS Major Scientific and Technological Project [XDA08010208]; NSFC [31071212, 91019008]
类目[WOS]: Biochemistry & Molecular Biology ; Cell Biology
研究领域[WOS]: Biochemistry & Molecular Biology ; Cell Biology
摘要: ELL (eleven-nineteen lysine-rich leukemia protein) was first identified as a translocation partner of MLL in acute myeloid leukemia; however, the exact mechanism of its action has remained elusive. In this study, we identified ELL as a direct downstream target gene of E2F1. Coimmunoprecipitation assays showed that ELL interacted with E2F1 in vitro and in vivo, leading to inhibition of E2F1 transcriptional activity. In addition, ELL enhanced E2F1 deacetylation via recruitment of histone deacetylase 1 (HDAC1). Notably, the MLL-ELL fusion protein lost the inhibitory role of ELL in E2F1 transcriptional activity. Furthermore, DNA damage induced ELL in an E2F1-dependent manner and ELL protected cells against E2F1-dependent apoptosis. Our findings not only connect ELL to E2F1 function and uncover a novel role of ELL in response to DNA damage but also provide an insight into the mechanism for MLL-ELL-associated leukemogenesis.
英文摘要: ELL (eleven-nineteen lysine-rich leukemia protein) was first identified as a translocation partner of MLL in acute myeloid leukemia; however, the exact mechanism of its action has remained elusive. In this study, we identified ELL as a direct downstream target gene of E2F1. Coimmunoprecipitation assays showed that ELL interacted with E2F1 in vitro and in vivo, leading to inhibition of E2F1 transcriptional activity. In addition, ELL enhanced E2F1 deacetylation via recruitment of histone deacetylase 1 (HDAC1). Notably, the MLL-ELL fusion protein lost the inhibitory role of ELL in E2F1 transcriptional activity. Furthermore, DNA damage induced ELL in an E2F1-dependent manner and ELL protected cells against E2F1-dependent apoptosis. Our findings not only connect ELL to E2F1 function and uncover a novel role of ELL in response to DNA damage but also provide an insight into the mechanism for MLL-ELL-associated leukemogenesis.
关键词[WOS]: RNA-POLYMERASE-II ; ELONGATION-FACTOR ELL ; MIXED-LINEAGE LEUKEMIA ; DNA-DAMAGE ; COMPLEX SEC ; CELL-DEATH ; MLL-ELL ; PROTEIN ; GENE ; TRANSACTIVATION
语种: 英语
WOS记录号: WOS:000330583000016
ISSN号: 0270-7306
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.ihb.ac.cn/handle/342005/20097
Appears in Collections:水生生物分子与细胞生物学研究中心_期刊论文

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作者单位: 1.Chinese Acad Sci, Inst Hydrobiol, Key Lab Aquat Biodivers & Conservat, Wuhan, Peoples R China

Recommended Citation:
Zhang, Wei; Ji, Wei; Liu, Xing; Ouyang, Gang; Xiao, Wuhan.ELL Inhibits E2F1 Transcriptional Activity by Enhancing E2F1 Deacetylation via Recruitment of Histone Deacetylase 1,MOLECULAR AND CELLULAR BIOLOGY,2014,34(4):765-775
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