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Conference Paper: A centrosomal target of HTLV-I Tax on the road to genome instability

TitleA centrosomal target of HTLV-I Tax on the road to genome instability
Authors
Issue Date2007
PublisherMary Ann Liebert, Inc Publishers. The Journal's web site is located at http://www.liebertpub.com/aid
Citation
The 13th International Conference on Human Retrovirology HTLV and Related Viruses, Hakone, Japan, 21-25 May 2007. In AIDS Research and Human Retroviruses, 2007, v. 23 n. 4, p. 595 How to Cite?
AbstractCentrosome abnormalities are the cause of genome instability that initiates leukemogenesis. HTLV-I-transformed ATL cells are genomically unstable, but the underlying mechanisms are not clear. We recently demonstrated that centrosome overduplication is frequent in ATL cells and that this phenotype is attributed to the expression of the viral oncoprotein Tax. A fraction of Tax was found in the centrosome, whereby it physically interacted with and inhibited TAX1BP2, a novel coiled-coil protein that is a component of the cellular machinery to block centrosome duplication. Silencing of TAX1BP2 by RNAi caused centrosome hyperamplification. The interaction of Tax with TAX1BP2 interfered with the centrosomal function of the latter, leading to centrosome overduplication as seen in TAX1BP2-depleted cells and ATL cells. Our findings suggest a new mechanism for HTLV-I-induced transformation in which the Tax oncoprotein targets a centrosomal protein causing centrosome-associated genomic instability and aneuploidy.
Persistent Identifierhttp://hdl.handle.net/10722/96679
ISSN
2015 Impact Factor: 1.949
2015 SCImago Journal Rankings: 1.024

 

DC FieldValueLanguage
dc.contributor.authorJin, Den_HK
dc.date.accessioned2010-09-25T16:41:20Z-
dc.date.available2010-09-25T16:41:20Z-
dc.date.issued2007en_HK
dc.identifier.citationThe 13th International Conference on Human Retrovirology HTLV and Related Viruses, Hakone, Japan, 21-25 May 2007. In AIDS Research and Human Retroviruses, 2007, v. 23 n. 4, p. 595-
dc.identifier.issn0889-2229-
dc.identifier.urihttp://hdl.handle.net/10722/96679-
dc.description.abstractCentrosome abnormalities are the cause of genome instability that initiates leukemogenesis. HTLV-I-transformed ATL cells are genomically unstable, but the underlying mechanisms are not clear. We recently demonstrated that centrosome overduplication is frequent in ATL cells and that this phenotype is attributed to the expression of the viral oncoprotein Tax. A fraction of Tax was found in the centrosome, whereby it physically interacted with and inhibited TAX1BP2, a novel coiled-coil protein that is a component of the cellular machinery to block centrosome duplication. Silencing of TAX1BP2 by RNAi caused centrosome hyperamplification. The interaction of Tax with TAX1BP2 interfered with the centrosomal function of the latter, leading to centrosome overduplication as seen in TAX1BP2-depleted cells and ATL cells. Our findings suggest a new mechanism for HTLV-I-induced transformation in which the Tax oncoprotein targets a centrosomal protein causing centrosome-associated genomic instability and aneuploidy.-
dc.languageengen_HK
dc.publisherMary Ann Liebert, Inc Publishers. The Journal's web site is located at http://www.liebertpub.com/aid-
dc.relation.ispartofAIDS Research and Human Retrovirusesen_HK
dc.titleA centrosomal target of HTLV-I Tax on the road to genome instabilityen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailJin, D: dyjin@hkucc.hku.hken_HK
dc.identifier.authorityJin, D=rp00452en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1089/aid.2007.9998-
dc.identifier.hkuros127311en_HK
dc.identifier.hkuros127315-

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