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Article: The interaction between EEN and Abi-1, two MLL fusion partners, and synaptojanin and dynamin: Implications for leukaemogenesis

TitleThe interaction between EEN and Abi-1, two MLL fusion partners, and synaptojanin and dynamin: Implications for leukaemogenesis
Authors
KeywordsAbi-1
EEN family
MLL
SH3 domain
Synaptojanin
Issue Date2000
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/leu
Citation
Leukemia, 2000, v. 14 n. 4, p. 594-601 How to Cite?
AbstractThe mixed lineage leukaemia gene, MLL (also called HRX,ALL-1) in acute leukaemia is fused to at least 16 identified partner genes that display diverse structural and biochemical properties. Using GST pull down and the yeast two hybrid system, we show that two different MLL fusion partners with SH3 domains, EEN and Abi-1, interact with dynamin and synaptojanin, both of which are involved in endocytosis. Synaptojanin, a member of the inositol phosphatase family that has recently been shown to regulate cell proliferation and survival, is also known to bind to Eps15, the mouse homologue of AF1p, another fusion partner of MLL. Expression studies show that synaptojanin is strongly expressed in bone marrow and immature leukaemic cell lines, very weakly in peripheral blood leukocytes and absent in Raji, a mature B cell line. We found that the SH3 domains of EEN and Abi-1 interact with different proline-rich domains of synaptojanin while the EH domains of Eps15 interact with the NPF motifs of synaptojanin. In vitro competitive binding assays demonstrate that EEN displays stronger binding affinity than Abi-1 and may compete with it for synaptojanin. These findings suggest a potential link between MLL fusion-mediated leukaemogenesis and the inositol-signalling pathway.
Persistent Identifierhttp://hdl.handle.net/10722/68178
ISSN
2015 Impact Factor: 12.104
2015 SCImago Journal Rankings: 5.142
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorSo, CWen_HK
dc.contributor.authorSo, CKCen_HK
dc.contributor.authorCheung, Nen_HK
dc.contributor.authorChew, SLen_HK
dc.contributor.authorSham, MHen_HK
dc.contributor.authorChan, LCen_HK
dc.date.accessioned2010-09-06T06:02:06Z-
dc.date.available2010-09-06T06:02:06Z-
dc.date.issued2000en_HK
dc.identifier.citationLeukemia, 2000, v. 14 n. 4, p. 594-601en_HK
dc.identifier.issn0887-6924en_HK
dc.identifier.urihttp://hdl.handle.net/10722/68178-
dc.description.abstractThe mixed lineage leukaemia gene, MLL (also called HRX,ALL-1) in acute leukaemia is fused to at least 16 identified partner genes that display diverse structural and biochemical properties. Using GST pull down and the yeast two hybrid system, we show that two different MLL fusion partners with SH3 domains, EEN and Abi-1, interact with dynamin and synaptojanin, both of which are involved in endocytosis. Synaptojanin, a member of the inositol phosphatase family that has recently been shown to regulate cell proliferation and survival, is also known to bind to Eps15, the mouse homologue of AF1p, another fusion partner of MLL. Expression studies show that synaptojanin is strongly expressed in bone marrow and immature leukaemic cell lines, very weakly in peripheral blood leukocytes and absent in Raji, a mature B cell line. We found that the SH3 domains of EEN and Abi-1 interact with different proline-rich domains of synaptojanin while the EH domains of Eps15 interact with the NPF motifs of synaptojanin. In vitro competitive binding assays demonstrate that EEN displays stronger binding affinity than Abi-1 and may compete with it for synaptojanin. These findings suggest a potential link between MLL fusion-mediated leukaemogenesis and the inositol-signalling pathway.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/leuen_HK
dc.relation.ispartofLeukemiaen_HK
dc.subjectAbi-1en_HK
dc.subjectEEN familyen_HK
dc.subjectMLLen_HK
dc.subjectSH3 domainen_HK
dc.subjectSynaptojaninen_HK
dc.subject.meshAdaptor Proteins, Signal Transducingen_HK
dc.subject.meshBinding Sitesen_HK
dc.subject.meshBinding, Competitiveen_HK
dc.subject.meshBlood Cells - metabolismen_HK
dc.subject.meshCell Transformation, Neoplastic - geneticsen_HK
dc.subject.meshCytoskeletal Proteinsen_HK
dc.subject.meshDNA-Binding Proteins - geneticsen_HK
dc.subject.meshDynaminsen_HK
dc.subject.meshGTP Phosphohydrolases - metabolismen_HK
dc.subject.meshGene Expression Profilingen_HK
dc.subject.meshHomeodomain Proteins - genetics - metabolismen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIntracellular Signaling Peptides and Proteinsen_HK
dc.subject.meshLeukemia - etiology - geneticsen_HK
dc.subject.meshMacromolecular Substancesen_HK
dc.subject.meshMolecular Sequence Dataen_HK
dc.subject.meshMultigene Familyen_HK
dc.subject.meshMyeloid-Lymphoid Leukemia Proteinen_HK
dc.subject.meshNerve Tissue Proteins - metabolismen_HK
dc.subject.meshOncogene Proteins, Fusion - geneticsen_HK
dc.subject.meshOrgan Specificityen_HK
dc.subject.meshPhosphoric Monoester Hydrolases - metabolismen_HK
dc.subject.meshProtein Bindingen_HK
dc.subject.meshProteins - genetics - metabolismen_HK
dc.subject.meshProto-Oncogenesen_HK
dc.subject.meshRNA, Messenger - biosynthesis - isolation & purificationen_HK
dc.subject.meshRecombinant Fusion Proteins - metabolismen_HK
dc.subject.meshSignal Transductionen_HK
dc.subject.meshTranscription Factorsen_HK
dc.subject.meshTranslocation, Geneticen_HK
dc.subject.meshTwo-Hybrid System Techniquesen_HK
dc.subject.meshsrc Homology Domainsen_HK
dc.titleThe interaction between EEN and Abi-1, two MLL fusion partners, and synaptojanin and dynamin: Implications for leukaemogenesisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0887-6924&volume=14&issue=4&spage=594&epage=601&date=2000&atitle=The+interaction+between+EEN+and+Abi-1,+two+MLL+fusion+partners,+and+synaptojanin+and+dynamin:+implications+for+leukaemogenesisen_HK
dc.identifier.emailSham, MH:mhsham@hkucc.hku.hken_HK
dc.identifier.emailChan, LC:chanlc@hkucc.hku.hken_HK
dc.identifier.authoritySham, MH=rp00380en_HK
dc.identifier.authorityChan, LC=rp00373en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid10764144-
dc.identifier.scopuseid_2-s2.0-0034119048en_HK
dc.identifier.hkuros50824en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034119048&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume14en_HK
dc.identifier.issue4en_HK
dc.identifier.spage594en_HK
dc.identifier.epage601en_HK
dc.identifier.isiWOS:000086406200006-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridSo, CW=7102919928en_HK
dc.identifier.scopusauthoridSo, CKC=7102919975en_HK
dc.identifier.scopusauthoridCheung, N=36803314200en_HK
dc.identifier.scopusauthoridChew, SL=7202524605en_HK
dc.identifier.scopusauthoridSham, MH=7003729109en_HK
dc.identifier.scopusauthoridChan, LC=7403540707en_HK

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