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J. Virol., 08 1996, 5731-5734, Vol 70, No. 8
Copyright © 1996, American Society for Microbiology

A cooperative interaction of human T-cell leukemia virus type 1 Tax with the p21 cyclin-dependent kinase inhibitor activates the human immunodeficiency virus type 1 enhancer

SF Parker, ND Perkins, SD Gitlin and GJ Nabel
Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor 48109-0650, USA.

Interactions between the Tax transactivator of human T-cell leukemia virus type 1 (HTLV-1) and a cell cycle regulatory protein have been examined. We report cooperative stimulation of human immunodeficiency virus type 1 gene expression by Tax and a regulator of cell cycle progression, the p21 cyclin-dependent kinase inhibitor (CKI). This cooperativity results from the effect of p21 on transcriptional coactivation by Tax-induced NF-kappaB. This effect was abrogated by a mutation in Tax which specifically eliminated NF-kappaB induction, was inhibitable by IkappaB-alpha, and was markedly reduced in human immunodeficiency virus reporter plasmids with mutant kappaB sites. These studies demonstrate that transcriptional activation by Tax is influenced by cell cycle regulatory proteins.

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