Abstract:
:Human T-cell leukemia virus type 1 (HTLV-1) encodes a 40-kDa Tax phosphoprotein. Tax is a transcriptional activator which modulates expression of the viral long terminal repeat and transcription of many cellular genes. Because Tax is a critical HTLV-1 factor which mediates viral transformation of T cells during the genesis of adult T-cell leukemia, it is important to understand the processes which can activate or inactivate Tax function. Here, we report that ubiquitination of Tax is a posttranscriptional mechanism which regulates Tax function. We show that ubiquitination does not target Tax for degradation by the proteasome. Rather, ubiquitin addition modifies Tax in a proteasome-independent manner from an active to a less-active transcriptional form.
journal_name
J Viroljournal_title
Journal of virologyauthors
Peloponese JM Jr,Iha H,Yedavalli VR,Miyazato A,Li Y,Haller K,Benkirane M,Jeang KTdoi
10.1128/JVI.78.21.11686-11695.2004subject
Has Abstractpub_date
2004-11-01 00:00:00pages
11686-95issue
21eissn
0022-538Xissn
1098-5514pii
78/21/11686journal_volume
78pub_type
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journal_title:Journal of virology
pub_type: 杂志文章
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journal_title:Journal of virology
pub_type: 杂志文章
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journal_title:Journal of virology
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更新日期:2006-04-01 00:00:00
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更新日期:1997-04-01 00:00:00
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journal_title:Journal of virology
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journal_title:Journal of virology
pub_type: 杂志文章
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更新日期:2014-03-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
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更新日期:2018-08-16 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.29.3.1107-1117.1979
更新日期:1979-03-01 00:00:00