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
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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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