FB1, an E2A fusion partner in childhood leukemia, interacts with U19/EAF2 and inhibits its transcriptional activity
文献类型:期刊论文
作者 | Jiang, Feng; Ai, Junkui; Xiao, Wuhan; Wang, Zhou |
刊名 | CANCER LETTERS
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出版日期 | 2007-08-18 |
卷号 | 253期号:2页码:265-272 |
关键词 | FB1 U19/EAF2 EAF1 ELL |
ISSN号 | 0304-3835 |
通讯作者 | Wang, Z, Univ Massachusetts, Sch Med, Howard Hughes Med Inst, Worcester, MA 01605 USA |
中文摘要 | Background: U19/EAF2 is a potential tumor suppressor exhibiting frequent down-regulation and allelic loss in advanced human prostate cancer specimens. U 19/EAF2 has also been identified as ELL-associated factor 2 (EAF2) based on its binding to ELL, a fusion partner of MLL in acute myeloid leukemia. U19/EAF2 is a putative transcription factor with a transactivation domain and capability of sequence-specific DNA binding. Methods: Yeast-two-hybrid-screening was used to identify U19/EAF2-binding partners. Co-immunoprecipitation and mammalian 1-hybrid assay were used to characterize a U19/EAF2-binding partner. Results: FB1, an E2A fusion partner in childhood leukemia, was identified as a binding-partner of U19/EAF2. FB1 also binds to EAF1, the only homologue of U19/EAF2. FB1 also interacts and co-localizes with ELL in the nucleus. Interestingly, FB1 inhibited the transcriptional activity of U19/EAF2 but not EAF1. Conclusions: FB1 is an important binding partner and a functional regulator of U19/EAF2, EAF1, and/or ELL. (c) 2007 Elsevier Ireland Ltd. All rights reserved. |
英文摘要 | Background: U19/EAF2 is a potential tumor suppressor exhibiting frequent down-regulation and allelic loss in advanced human prostate cancer specimens. U 19/EAF2 has also been identified as ELL-associated factor 2 (EAF2) based on its binding to ELL, a fusion partner of MLL in acute myeloid leukemia. U19/EAF2 is a putative transcription factor with a transactivation domain and capability of sequence-specific DNA binding. |
WOS标题词 | Science & Technology ; Life Sciences & Biomedicine |
学科主题 | Oncology |
类目[WOS] | Oncology |
研究领域[WOS] | Oncology |
关键词[WOS] | FACTOR-2 EAF2 ; ELL ; GENE ; PROTEIN ; AMIDA ; APOPTOSIS ; GROWTH ; MLL ; IDENTIFICATION ; LOCALIZATION |
收录类别 | SCI |
语种 | 英语 |
WOS记录号 | WOS:000248612200010 |
公开日期 | 2010-10-13 |
源URL | [http://ir.ihb.ac.cn/handle/152342/8524] ![]() |
专题 | 水生生物研究所_中科院水生所知识产出(2009年前)_期刊论文 |
作者单位 | 1.Univ Pittsburgh, Sch Med, Inst Canc, Dept Urol, Pittsburgh, PA 15232 USA 2.Univ Massachusetts, Sch Med, Program Mol Med, Worcester, MA 01605 USA 3.Northwestern Univ, Feinberg Sch Med, Dept Urol, Chicago, IL 60611 USA 4.Northwestern Univ, Feinberg Sch Med, Dept Mol Pharmacol & Biol Chem, Chicago, IL 60611 USA 5.Northwestern Univ, Feinberg Sch Med, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA 6.Chinese Acad Sci, Inst Hydrobiol, Wuhan 430072, Peoples R China |
推荐引用方式 GB/T 7714 | Jiang, Feng,Ai, Junkui,Xiao, Wuhan,et al. FB1, an E2A fusion partner in childhood leukemia, interacts with U19/EAF2 and inhibits its transcriptional activity[J]. CANCER LETTERS,2007,253(2):265-272. |
APA | Jiang, Feng,Ai, Junkui,Xiao, Wuhan,&Wang, Zhou.(2007).FB1, an E2A fusion partner in childhood leukemia, interacts with U19/EAF2 and inhibits its transcriptional activity.CANCER LETTERS,253(2),265-272. |
MLA | Jiang, Feng,et al."FB1, an E2A fusion partner in childhood leukemia, interacts with U19/EAF2 and inhibits its transcriptional activity".CANCER LETTERS 253.2(2007):265-272. |
入库方式: OAI收割
来源:水生生物研究所
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