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Article: The retroviral oncoprotein Tax targets the coiled-coil centrosomal protein TAX1BP2 to induce centrosome overduplication

TitleThe retroviral oncoprotein Tax targets the coiled-coil centrosomal protein TAX1BP2 to induce centrosome overduplication
Authors
Issue Date2006
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/naturecellbiology
Citation
Nature Cell Biology, 2006, v. 8 n. 7, p. 717-724 How to Cite?
AbstractEmerging evidence suggests that supernumerary centrosomes drive genome instability and oncogenesis. Human T-cell leukaemia virus type I (HTLV-I) is etiologically associated with adult T-cell leukaemia (ATL). ATL cells are aneuploid, but the causes of aneuploidy are incompletely understood. Here, we show that centrosome amplification is frequent in HTLV-I-transformed cells and that this phenotype is caused by the viral Tax oncoprotein. We also show that the fraction of Tax protein that localizes to centrosomes interacts with TAX1BP2, a novel centrosomal protein composed almost entirely of coiled-coil domains. Overexpression of TAX1BP2 inhibited centrosome duplication, whereas depletion of TAX1BP2 by RNAi resulted in centrosome hyperamplification. Our findings suggest that the HTLV-I Tax oncoprotein targets TAX1BP2 causing genomic instability and aneuploidy. © 2006 Nature Publishing Group.
Persistent Identifierhttp://hdl.handle.net/10722/54244
ISSN
2015 Impact Factor: 18.699
2015 SCImago Journal Rankings: 14.131
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChing, YPen_HK
dc.contributor.authorChan, SFen_HK
dc.contributor.authorJeang, KTen_HK
dc.contributor.authorJin, DYen_HK
dc.date.accessioned2009-04-03T07:40:55Z-
dc.date.available2009-04-03T07:40:55Z-
dc.date.issued2006en_HK
dc.identifier.citationNature Cell Biology, 2006, v. 8 n. 7, p. 717-724en_HK
dc.identifier.issn1465-7392en_HK
dc.identifier.urihttp://hdl.handle.net/10722/54244-
dc.description.abstractEmerging evidence suggests that supernumerary centrosomes drive genome instability and oncogenesis. Human T-cell leukaemia virus type I (HTLV-I) is etiologically associated with adult T-cell leukaemia (ATL). ATL cells are aneuploid, but the causes of aneuploidy are incompletely understood. Here, we show that centrosome amplification is frequent in HTLV-I-transformed cells and that this phenotype is caused by the viral Tax oncoprotein. We also show that the fraction of Tax protein that localizes to centrosomes interacts with TAX1BP2, a novel centrosomal protein composed almost entirely of coiled-coil domains. Overexpression of TAX1BP2 inhibited centrosome duplication, whereas depletion of TAX1BP2 by RNAi resulted in centrosome hyperamplification. Our findings suggest that the HTLV-I Tax oncoprotein targets TAX1BP2 causing genomic instability and aneuploidy. © 2006 Nature Publishing Group.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/naturecellbiologyen_HK
dc.relation.ispartofNature Cell Biologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshAneuploidyen_HK
dc.subject.meshCell Transformation, Neoplastic - genetics - metabolismen_HK
dc.subject.meshCercopithecus aethiopsen_HK
dc.subject.meshGene Products, tax - genetics - metabolismen_HK
dc.subject.meshGenomic Instability - physiologyen_HK
dc.titleThe retroviral oncoprotein Tax targets the coiled-coil centrosomal protein TAX1BP2 to induce centrosome overduplicationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1465-7392&volume=8&issue=7&spage=717&epage=724&date=2006&atitle=Retroviral+oncoprotein+Tax+targets+coiled-coil+centrosomal+protein+TAX1BP2+to+induce+centrosome+overduplication.en_HK
dc.identifier.emailChing, YP:ypching@hku.hken_HK
dc.identifier.emailJin, DY:dyjin@hkucc.hku.hken_HK
dc.identifier.authorityChing, YP=rp00469en_HK
dc.identifier.authorityJin, DY=rp00452en_HK
dc.description.naturepostprinten_HK
dc.identifier.doi10.1038/ncb1432en_HK
dc.identifier.pmid16767081en_HK
dc.identifier.scopuseid_2-s2.0-33745741138en_HK
dc.identifier.hkuros119563-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33745741138&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume8en_HK
dc.identifier.issue7en_HK
dc.identifier.spage717en_HK
dc.identifier.epage724en_HK
dc.identifier.eissn1476-4679-
dc.identifier.isiWOS:000238837800014-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridChing, YP=7005431277en_HK
dc.identifier.scopusauthoridChan, SF=7404255795en_HK
dc.identifier.scopusauthoridJeang, KT=7004824803en_HK
dc.identifier.scopusauthoridJin, DY=7201973614en_HK
dc.identifier.citeulike745967-

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