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PMID: 2309119 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

HTLV-I trans-activator protein, tax, is a trans-repressor of the human beta-polymerase gene.

Science (New York, N.Y.) ·Vol. 247 ·No. 4946 ·1990-03-02 ·Pages 1082-4

Jeang KT, Widen SG, Semmes OJ, Wilson SH

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.

MeSH Terms
Base Sequence Cell Line Cell Line, Transformed DNA Polymerase I/genetics DNA, Viral/genetics Gene Expression Regulation, Enzymologic Gene Expression Regulation, Viral Human T-lymphotropic virus 1/genetics Humans Molecular Sequence Data Plasmids Promoter Regions, Genetic RNA, Messenger/biosynthesis Repetitive Sequences, Nucleic Acid Repressor Proteins/biosynthesis,genetics Trans-Activators/biosynthesis,genetics Transcription Factors/genetics Transfection
Chemicals
DNA, Viral RNA, Messenger Repressor Proteins Trans-Activators Transcription Factors DNA Polymerase I
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Jeang K T
Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.
Widen S G
Semmes O J
Wilson S H
Article Info
Journal
Science (New York, N.Y.)
Abbr.
Science
ISSN
0036-8075
Published
1990-03-02
Pages
1082-4
Language
English
Region
United States
NLM ID
0404511
Subset
IM
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