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在稳定表达I型人类嗜T细胞病毒Tax蛋白的T细胞中的核因子-κB活性

NF-kappa B activity in T cells stably expressing the Tax protein of human T cell lymphotropic virus type I.

作者信息

Lacoste J, Cohen L, Hiscott J

机构信息

Lady Davis Institute for Medical Research, Sir Mortimer B. Davis-Jewish General Hospital, Montreal, Quebec, Canada.

出版信息

Virology. 1991 Oct;184(2):553-62. doi: 10.1016/0042-6822(91)90425-b.

DOI:10.1016/0042-6822(91)90425-b
PMID:1679576
Abstract

The effect of constitutive Tax expression on the interaction of NF-kappa B with its recognition sequence and on NF-kappa B-dependent gene expression was examined in T lymphoid Jurkat cell lines (19D and 9J) stably transformed with a Tax expression vector. Tax expressing T cell lines contained a constitutive level of NF-kappa B binding activity, detectable by mobility shift assay and uv cross-linking using a palindromic NF-kappa B probe homologous to the interferon beta PRDII site. In Jurkat and NC2.10 induction with phorbol esters resulted in the appearance of new DNA binding proteins of 85, 75, and 54 kDa, whereas in Tax expressing cells the 85-kDa protein and a 92-kDa DNA binding protein were constitutively induced. Expression of Tax protein in 19D and 9J resulted in transcription of the endogenous NF-kappa B-dependent granulocyte-macrophage colony stimulating factor gene and increased basal level expression of transfected NF-kappa B-regulated promoters. Nonetheless transcription of both the endogenous and the transfected gene was inducible by PMA treatment. Tax expression in Jurkat T cells may alter the stoichiometry of NF-kappa B DNA binding proteins and thus change the expression of NF-kappa B-regulated promoters.

摘要

在稳定转染了Tax表达载体的T淋巴细胞Jurkat细胞系(19D和9J)中,研究了组成型Tax表达对NF-κB与其识别序列相互作用以及对NF-κB依赖性基因表达的影响。表达Tax的T细胞系含有组成型水平的NF-κB结合活性,可通过迁移率变动分析和使用与干扰素βPRDII位点同源的回文NF-κB探针进行紫外线交联检测到。在Jurkat和NC2.10中,佛波酯诱导导致出现85、75和54 kDa的新DNA结合蛋白,而在表达Tax的细胞中,85 kDa蛋白和92 kDa DNA结合蛋白是组成型诱导的。19D和9J中Tax蛋白的表达导致内源性NF-κB依赖性粒细胞-巨噬细胞集落刺激因子基因的转录,并增加了转染的NF-κB调控启动子的基础水平表达。尽管如此,内源性和转染基因的转录均可通过PMA处理诱导。Jurkat T细胞中Tax的表达可能会改变NF-κB DNA结合蛋白的化学计量,从而改变NF-κB调控启动子的表达。

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