人类T细胞白血病病毒1型Tax与p21细胞周期蛋白依赖性激酶抑制剂的协同相互作用激活了人类免疫缺陷病毒1型增强子。
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.
作者信息
Parker S F, Perkins N D, Gitlin S D, Nabel G J
机构信息
Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor 48109-0650, USA.
出版信息
J Virol. 1996 Aug;70(8):5731-4. doi: 10.1128/JVI.70.8.5731-5734.1996.
Abstract
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.
摘要
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。
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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.人类T细胞白血病病毒1型Tax与p21细胞周期蛋白依赖性激酶抑制剂的协同相互作用激活了人类免疫缺陷病毒1型增强子。
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