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FB1, an E2A fusion partner in childhood leukemia, interacts with U19/EAF2 and inhibits its transcriptional activity
Jiang, Feng; Ai, Junkui; Xiao, Wuhan; Wang, Zhou; Wang, Z, Univ Massachusetts, Sch Med, Howard Hughes Med Inst, Worcester, MA 01605 USA
2007-08-18
Source PublicationCANCER LETTERS
ISSN0304-3835
Volume253Issue:2Pages:265-272
AbstractBackground: 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.; 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.
SubtypeArticle
KeywordFb1 U19/eaf2 Eaf1 Ell
DepartmentUniv Pittsburgh, Sch Med, Inst Canc, Dept Urol, Pittsburgh, PA 15232 USA; Univ Massachusetts, Sch Med, Program Mol Med, Worcester, MA 01605 USA; Northwestern Univ, Feinberg Sch Med, Dept Urol, Chicago, IL 60611 USA; Northwestern Univ, Feinberg Sch Med, Dept Mol Pharmacol & Biol Chem, Chicago, IL 60611 USA; Northwestern Univ, Feinberg Sch Med, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA; Chinese Acad Sci, Inst Hydrobiol, Wuhan 430072, Peoples R China
Subject AreaOncology
DOI10.1016/j.canlet.2007.02.003
WOS HeadingsScience & Technology ; Life Sciences & Biomedicine
Indexed BySCI
Language英语
WOS Research AreaOncology
WOS SubjectOncology
WOS IDWOS:000248612200010
WOS KeywordFACTOR-2 EAF2 ; ELL ; GENE ; PROTEIN ; AMIDA ; APOPTOSIS ; GROWTH ; MLL ; IDENTIFICATION ; LOCALIZATION
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Cited Times:4[WOS]   [WOS Record]     [Related Records in WOS]
Document Type期刊论文
Identifierhttp://ir.ihb.ac.cn/handle/152342/8524
Collection期刊论文
Corresponding AuthorWang, Z, Univ Massachusetts, Sch Med, Howard Hughes Med Inst, Worcester, MA 01605 USA
Affiliation1.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
Recommended Citation
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,&Wang, Z, Univ Massachusetts, Sch Med, Howard Hughes Med Inst, Worcester, MA 01605 USA.(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.
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