Abstract:
:The Tax protein from human T-cell leukemia virus type I (HTLV-I) is a 40-kDa phosphoprotein capable of activating transcription from its own long terminal repeat (LTR), as well as increasing the transcription of cellular genes. Transcriptional activation of the HTLV-I LTR has been demonstrated via a cyclic-AMP-responsive element within the 21-bp Tax-responsive elements of the LTR. Phorbol esters also upregulate expression via the LTR. Since phosphorylation of Tax may play a role in these processes, we investigated the relative effects of kinase-stimulating agents on 32P incorporation into Tax. Our studies demonstrated that the phorbol ester 4 beta-phorbol-12 beta-myristate-13 alpha-acetate greatly stimulated Tax phosphorylation in a time- and dose-dependent manner. In contrast, 8-bromoadenosine 3'-5'-cyclic monophosphate induced little stimulation of Tax phosphorylation. Tax phosphorylation occurred only on serine residues and was mapped to a single tryptic fragment in both Tax-producing human lymphocytes and mouse fibroblast cells.
journal_name
J Viroljournal_title
Journal of virologyauthors
Fontes JD,Strawhecker JM,Bills ND,Lewis RE,Hinrichs SHdoi
10.1128/JVI.67.7.4436-4441.1993subject
Has Abstractpub_date
1993-07-01 00:00:00pages
4436-41issue
7eissn
0022-538Xissn
1098-5514journal_volume
67pub_type
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更新日期:1979-11-01 00:00:00
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pub_type: 杂志文章
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更新日期:2009-04-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
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pub_type: 杂志文章
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更新日期:1999-07-01 00:00:00
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journal_title:Journal of virology
pub_type: 杂志文章
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pub_type: 杂志文章
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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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更新日期:1977-01-01 00:00:00
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pub_type: 杂志文章
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pub_type: 杂志文章
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