中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
ELL Inhibits E2F1 Transcriptional Activity by Enhancing E2F1 Deacetylation via Recruitment of Histone Deacetylase 1

文献类型:期刊论文

作者Zhang, Wei; Ji, Wei; Liu, Xing; Ouyang, Gang; Xiao, Wuhan
刊名MOLECULAR AND CELLULAR BIOLOGY
出版日期2014-02-01
卷号34期号:4页码:765-775
关键词RNA-POLYMERASE-II ELONGATION-FACTOR ELL MIXED-LINEAGE LEUKEMIA DNA-DAMAGE COMPLEX SEC CELL-DEATH MLL-ELL PROTEIN GENE TRANSACTIVATION
ISSN号0270-7306
通讯作者Xiao, WH (reprint author), Chinese Acad Sci, Inst Hydrobiol, Key Lab Aquat Biodivers & Conservat, Wuhan, Peoples R China.
中文摘要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.
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.
WOS标题词Science & Technology ; Life Sciences & Biomedicine
类目[WOS]Biochemistry & Molecular Biology ; Cell Biology
研究领域[WOS]Biochemistry & Molecular Biology ; Cell Biology
关键词[WOS]RNA-POLYMERASE-II ; ELONGATION-FACTOR ELL ; MIXED-LINEAGE LEUKEMIA ; DNA-DAMAGE ; COMPLEX SEC ; CELL-DEATH ; MLL-ELL ; PROTEIN ; GENE ; TRANSACTIVATION
收录类别SCI
资助信息973 grant [2010CB126306]; CAS Major Scientific and Technological Project [XDA08010208]; NSFC [31071212, 91019008]
语种英语
WOS记录号WOS:000330583000016
公开日期2014-08-13
源URL[http://ir.ihb.ac.cn/handle/342005/20097]  
专题水生生物研究所_水生生物分子与细胞生物学研究中心_期刊论文
作者单位Chinese Acad Sci, Inst Hydrobiol, Key Lab Aquat Biodivers & Conservat, Wuhan, Peoples R China
推荐引用方式
GB/T 7714
Zhang, Wei,Ji, Wei,Liu, Xing,et al. ELL Inhibits E2F1 Transcriptional Activity by Enhancing E2F1 Deacetylation via Recruitment of Histone Deacetylase 1[J]. MOLECULAR AND CELLULAR BIOLOGY,2014,34(4):765-775.
APA Zhang, Wei,Ji, Wei,Liu, Xing,Ouyang, Gang,&Xiao, Wuhan.(2014).ELL Inhibits E2F1 Transcriptional Activity by Enhancing E2F1 Deacetylation via Recruitment of Histone Deacetylase 1.MOLECULAR AND CELLULAR BIOLOGY,34(4),765-775.
MLA Zhang, Wei,et al."ELL Inhibits E2F1 Transcriptional Activity by Enhancing E2F1 Deacetylation via Recruitment of Histone Deacetylase 1".MOLECULAR AND CELLULAR BIOLOGY 34.4(2014):765-775.

入库方式: OAI收割

来源:水生生物研究所

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