Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2002-5-23
pubmed:abstractText
Our aim was to examine the involvement of G(1) cell-cycle regulators in cell growth dysregulation induced by HTLV-I. Compared to uninfected cells, higher expression levels of cyclin D1 and D2 mRNA were detected in HTLV-I-infected T-cell lines, which were at least in part mediated by the viral transforming protein Tax since Tax activated both cyclin D1 and D2 promoters in the human T-cell line Jurkat. A Tax mutant that did not activate NF-kappaB failed to activate cyclin D1 and D2 promoters. Inhibitors of NF-kappaB (dominant negative IkappaBs mutants) suppressed Tax-dependent activation of cyclin D1 and D2 promoters, indicating that Tax-induced activation was mediated by NF-kappaB. Wild-type and mutant Tax capable of activating NF-kappaB, but not Tax mutant incapable of activating NF-kappaB, converted cell growth of a T-cell line from being IL-2-dependent to being IL-2-independent; and this conversion was associated with IL-2-independent induction of cyclins D1 and D2. Our data suggest that induction of cyclins D1 and D2 by Tax is involved in IL-2-independent cell-cycle progression as well as IL-2-independent transformation of primary human T cells by HTLV-I. High expression levels of cyclin D1 and D2 mRNAs were also detected in some patients with ATL. Our findings link HTLV-I infection to changes in cellular D-type cyclin gene expression, transformation of T cells and subsequent development of T-cell leukemia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0020-7136
pubmed:author
pubmed:copyrightInfo
Copyright 2002 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
99
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
378-85
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:11992406-Animals, pubmed-meshheading:11992406-Blotting, Northern, pubmed-meshheading:11992406-Blotting, Western, pubmed-meshheading:11992406-Cell Cycle, pubmed-meshheading:11992406-Cell Division, pubmed-meshheading:11992406-Cyclin D1, pubmed-meshheading:11992406-Cyclin D2, pubmed-meshheading:11992406-Cyclins, pubmed-meshheading:11992406-Gene Products, tax, pubmed-meshheading:11992406-Humans, pubmed-meshheading:11992406-Interleukin-2, pubmed-meshheading:11992406-Kinetics, pubmed-meshheading:11992406-Leukemia, T-Cell, pubmed-meshheading:11992406-Mice, pubmed-meshheading:11992406-NF-kappa B, pubmed-meshheading:11992406-Plasmids, pubmed-meshheading:11992406-Promoter Regions, Genetic, pubmed-meshheading:11992406-RNA, Messenger, pubmed-meshheading:11992406-T-Lymphocytes, pubmed-meshheading:11992406-Transcription, Genetic, pubmed-meshheading:11992406-Transcriptional Activation, pubmed-meshheading:11992406-Transfection, pubmed-meshheading:11992406-Tumor Cells, Cultured
pubmed:year
2002
pubmed:articleTitle
Activation of cyclin D1 and D2 promoters by human T-cell leukemia virus type I tax protein is associated with IL-2-independent growth of T cells.
pubmed:affiliation
Department of Preventive Medicine and AIDS Research, Institute of Tropical Medicine, Nagasaki University, Nagasaki, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't