Publication Date:
1990-03-02
Description:
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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jeang, K T -- Widen, S G -- Semmes, O J 4th -- Wilson, S H -- New York, N.Y. -- Science. 1990 Mar 2;247(4946):1082-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2309119" target="_blank"〉PubMed〈/a〉
Keywords:
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
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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