巨噬细胞中Ets、rel和sp1样蛋白参与脂多糖介导的HIV-1 LTR活化

Journal of inflammation Pub Date : 1998-01-01
M J Sweet, K J Stacey, I L Ross, M C Ostrowski, D A Hume
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引用次数: 0

摘要

HIV-1启动子被用作模型来鉴定RAW 264小鼠巨噬细胞中参与lps依赖性转录的转录因子。Ets-2和PU.1的表达质粒反式激活了HIV-1 LTR和重组PU.1,以及与HIV-1增强子5' kappa B位点结合的Ets-2 DNA结合域/GST融合蛋白。在RAW 264细胞中,LPS可诱导Ets-2 mRNA, LPS可刺激Ets-2尖结构域中苏氨酸72残基的磷酸化。在添加质粒DNA时,也观察到Ets-2和其他lps应答转录因子的诱导,这使得瞬时转染的解释变得复杂。含有两个Sp1位点的近端启动子区域也对lps有反应。我们认为kappa B元件和串联Sp1位点作为LPS响应元件,kappa B介导的LPS作用涉及et和rel因子。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Involvement of Ets, rel and Sp1-like proteins in lipopolysaccharide-mediated activation of the HIV-1 LTR in macrophages.

The HIV-1 promoter was used as a model to identify transcription factors involved in LPS-dependent transcription in RAW 264 murine macrophages. Expression plasmids for Ets-2 and PU.1 trans-activated the HIV-1 LTR and recombinant PU.1 and an Ets-2 DNA binding domain/GST fusion protein bound to the 5' kappa B site of the HIV-1 enhancer. Ets-2 mRNA was LPS-inducible in RAW 264 cells and LPS stimulated phosphorylation of threonine 72 residue within the Ets-2 pointed domain. Induction of Ets-2 and other LPS-responsive transcription factors was also observed upon addition of plasmid DNA, which complicates interpretation of transient transfections. The proximal promoter region, containing two Sp1 sites, was also LPS-responsive. We propose that the kappa B elements and the tandem Sp1 sites act as LPS response elements and that kappa B-mediated LPS action involves Ets and rel factors.

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