牛白血病病毒启动子中NF-κB结合位点的鉴定。
Identification of an NF-kappa B binding site in the bovine leukemia virus promoter.
作者信息
Brooks P A, Nyborg J K, Cockerell G L
机构信息
Department of Pathology, Colorado State University, Fort Collins 80523, USA.
出版信息
J Virol. 1995 Oct;69(10):6005-9. doi: 10.1128/JVI.69.10.6005-6009.1995.
Abstract
Although the mechanism by which bovine leukemia virus (BLV) induces neoplastic transformation of the host B cells is unknown, it is likely that critical interactions between cellular DNA-binding proteins and the virus are involved. We have used DNase I protection (footprinting) assays to construct a map of protein-DNA interactions on the 5' long terminal repeat of BLV. In addition to the three cyclic AMP response elements previously reported, we have also found an NF-kappa B binding site between -118 and -70 nucleotides upstream of the RNA start site. This site binds several members of the kappa B family of proteins, including p49, p50, and p65, in both footprint and electrophoretic mobility shift assays and functions as an enhancer element when inserted upstream of the chloramphenicol acetyltransferase gene. NF-kappa B may be a critical nuclear binding protein that regulates both viral replication and key cellular genes in BLV-infected B cells.
摘要
尽管牛白血病病毒（BLV）诱导宿主B细胞发生肿瘤转化的机制尚不清楚，但细胞DNA结合蛋白与该病毒之间的关键相互作用可能参与其中。我们利用DNA酶I保护（足迹法）分析构建了BLV 5'长末端重复序列上蛋白质-DNA相互作用图谱。除了先前报道的三个环磷酸腺苷反应元件外，我们还在RNA起始位点上游-118至-70核苷酸之间发现了一个核因子κB（NF-κB）结合位点。在足迹法和电泳迁移率变动分析中，该位点能结合κB家族的几种蛋白质成员，包括p49、p50和p65，并且当插入氯霉素乙酰转移酶基因上游时可作为增强子元件发挥作用。NF-κB可能是一种关键的核结合蛋白，它在BLV感染的B细胞中调节病毒复制和关键细胞基因。
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