Parker S F, Perkins N D, Gitlin S D, Nabel G J
Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor 48109-0650, USA.
J Virol. 1996 Aug;70(8):5731-4. doi: 10.1128/JVI.70.8.5731-5734.1996.
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.
对人类1型T细胞白血病病毒（HTLV-1）的反式激活蛋白Tax与一种细胞周期调节蛋白之间的相互作用进行了研究。我们报告了Tax和细胞周期进程调节因子p21细胞周期蛋白依赖性激酶抑制剂（CKI）对人类免疫缺陷病毒1型基因表达的协同刺激作用。这种协同作用源于p21对Tax诱导的核因子κB（NF-κB）转录共激活的影响。Tax中一个特异性消除NF-κB诱导的突变消除了这种作用，该作用可被IκB-α抑制，并且在具有突变κB位点的人类免疫缺陷病毒报告质粒中显著降低。这些研究表明，Tax的转录激活受到细胞周期调节蛋白的影响。
