Abstract
Human T cell leukemia virus type I (HTLV-I) is the etiological agent for adult T cell leukemia (ATL). The HTLV-I trans-activator protein Tax can activate the expression of its own long terminal repeat (LTR) and many cellular and viral genes. Tax down-regulated the expression of human beta-polymerase (hu beta-pol), a cellular enzyme involved in host cell DNA repair. This finding suggests a possible correlation between HTLV-I infection and host chromosomal damage, which is often seen in ATL cells.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Base Sequence
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Cell Line
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Cell Line, Transformed
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DNA Polymerase I / genetics*
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DNA, Viral / genetics
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Gene Expression Regulation, Enzymologic
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Gene Expression Regulation, Viral
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Human T-lymphotropic virus 1 / genetics*
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Humans
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Molecular Sequence Data
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Plasmids
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Promoter Regions, Genetic
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RNA, Messenger / biosynthesis
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Repetitive Sequences, Nucleic Acid
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Repressor Proteins / biosynthesis
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Repressor Proteins / genetics*
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Trans-Activators / biosynthesis
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Trans-Activators / genetics*
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Transcription Factors / genetics*
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Transfection
Substances
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DNA, Viral
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RNA, Messenger
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Repressor Proteins
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Trans-Activators
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Transcription Factors
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DNA Polymerase I