IHB OpenIR  > 水生生物分子与细胞生物学研究中心  > 期刊论文
ELL Inhibits E2F1 Transcriptional Activity by Enhancing E2F1 Deacetylation via Recruitment of Histone Deacetylase 1
Zhang, Wei; Ji, Wei; Liu, Xing; Ouyang, Gang; Xiao, Wuhan; Xiao, WH (reprint author), Chinese Acad Sci, Inst Hydrobiol, Key Lab Aquat Biodivers & Conservat, Wuhan, Peoples R China.
2014-02-01
Source PublicationMOLECULAR AND CELLULAR BIOLOGY
ISSN0270-7306
Volume34Issue:4Pages:765-775
AbstractELL (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.; 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.
SubtypeArticle
KeywordRna-polymerase-ii Elongation-factor Ell Mixed-lineage Leukemia Dna-damage Complex Sec Cell-death Mll-ell Protein Gene Transactivation
Department[Zhang, Wei; Ji, Wei; Liu, Xing; Ouyang, Gang; Xiao, Wuhan] Chinese Acad Sci, Inst Hydrobiol, Key Lab Aquat Biodivers & Conservat, Wuhan, Peoples R China
DOI10.1128/MCB.00878-13
WOS HeadingsScience & Technology ; Life Sciences & Biomedicine
Funding Organization973 grant [2010CB126306]; CAS Major Scientific and Technological Project [XDA08010208]; NSFC [31071212, 91019008] ; 973 grant [2010CB126306]; CAS Major Scientific and Technological Project [XDA08010208]; NSFC [31071212, 91019008] ; 973 grant [2010CB126306]; CAS Major Scientific and Technological Project [XDA08010208]; NSFC [31071212, 91019008] ; 973 grant [2010CB126306]; CAS Major Scientific and Technological Project [XDA08010208]; NSFC [31071212, 91019008]
Indexed BySCI
Language英语
WOS Research AreaBiochemistry & Molecular Biology ; Cell Biology
WOS SubjectBiochemistry & Molecular Biology ; Cell Biology
WOS IDWOS:000330583000016
WOS KeywordRNA-POLYMERASE-II ; ELONGATION-FACTOR ELL ; MIXED-LINEAGE LEUKEMIA ; DNA-DAMAGE ; COMPLEX SEC ; CELL-DEATH ; MLL-ELL ; PROTEIN ; GENE ; TRANSACTIVATION
Funding Organization973 grant [2010CB126306]; CAS Major Scientific and Technological Project [XDA08010208]; NSFC [31071212, 91019008] ; 973 grant [2010CB126306]; CAS Major Scientific and Technological Project [XDA08010208]; NSFC [31071212, 91019008] ; 973 grant [2010CB126306]; CAS Major Scientific and Technological Project [XDA08010208]; NSFC [31071212, 91019008] ; 973 grant [2010CB126306]; CAS Major Scientific and Technological Project [XDA08010208]; NSFC [31071212, 91019008]
Citation statistics
Document Type期刊论文
Identifierhttp://ir.ihb.ac.cn/handle/342005/20097
Collection水生生物分子与细胞生物学研究中心_期刊论文
Corresponding AuthorXiao, WH (reprint author), Chinese Acad Sci, Inst Hydrobiol, Key Lab Aquat Biodivers & Conservat, Wuhan, Peoples R China.
AffiliationChinese Acad Sci, Inst Hydrobiol, Key Lab Aquat Biodivers & Conservat, Wuhan, Peoples R China
Recommended Citation
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,&Xiao, WH .(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.
Files in This Item:
File Name/Size DocType Version Access License
ELL Inhibits E2F1 Tr(3670KB) 开放获取CC BY-NC-SAView Application Full Text
Related Services
Recommend this item
Bookmark
Usage statistics
Export to Endnote
Google Scholar
Similar articles in Google Scholar
[Zhang, Wei]'s Articles
[Ji, Wei]'s Articles
[Liu, Xing]'s Articles
Baidu academic
Similar articles in Baidu academic
[Zhang, Wei]'s Articles
[Ji, Wei]'s Articles
[Liu, Xing]'s Articles
Bing Scholar
Similar articles in Bing Scholar
[Zhang, Wei]'s Articles
[Ji, Wei]'s Articles
[Liu, Xing]'s Articles
Terms of Use
No data!
Social Bookmark/Share
File name: ELL Inhibits E2F1 Transcriptional Activity by Enhancing E2F1 Deacetylation via Recruitment of Histone Deacetylase 1.pdf
Format: Adobe PDF
This file does not support browsing at this time
All comments (0)
No comment.
 

Items in the repository are protected by copyright, with all rights reserved, unless otherwise indicated.