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本文引用的文献

1
The inducible transcription factor NF-kappa B: structure-function relationship of its protein subunits.诱导型转录因子核因子-κB:其蛋白质亚基的结构-功能关系
Biochem J. 1993 Mar 1;290 ( Pt 2)(Pt 2):297-308. doi: 10.1042/bj2900297.
2
Transactivation by the human T-cell leukemia virus Tax protein is mediated through enhanced binding of activating transcription factor-2 (ATF-2) ATF-2 response and cAMP element-binding protein (CREB).人类T细胞白血病病毒Tax蛋白的反式激活作用是通过增强激活转录因子2(ATF-2)、ATF-2反应元件和环磷酸腺苷反应元件结合蛋白(CREB)的结合来介导的。
J Biol Chem. 1993 Oct 5;268(28):21225-31.
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Pleiotropic effect of the human T-cell leukemia virus Tax protein on the DNA binding activity of eukaryotic transcription factors.人类T细胞白血病病毒Tax蛋白对真核转录因子DNA结合活性的多效性作用。
Proc Natl Acad Sci U S A. 1993 Aug 1;90(15):7303-7. doi: 10.1073/pnas.90.15.7303.
4
Nuclear factor kappa B, a mediator of lipopolysaccharide effects.核因子κB,脂多糖效应的介质。
Immunobiology. 1993 Apr;187(3-5):233-56. doi: 10.1016/S0171-2985(11)80342-6.
5
A novel NF-kappa B complex containing p65 homodimers: implications for transcriptional control at the level of subunit dimerization.一种包含p65同型二聚体的新型核因子-κB复合物:对亚基二聚化水平转录调控的影响。
Mol Cell Biol. 1993 Dec;13(12):7826-35. doi: 10.1128/mcb.13.12.7826-7835.1993.
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Tax protein of human T-lymphotropic virus type I triggers DNA damage.人类嗜T淋巴细胞病毒I型的Tax蛋白引发DNA损伤。
Leuk Lymphoma. 1994 Jan;12(3-4):281-6. doi: 10.3109/10428199409059600.
7
Characterization of NF(P), the nuclear factor that interacts with the regulatory P sequence (5'-CGAAAATTTCC-3') of the human interleukin-4 gene: relationship to NF-kappa B and NF-AT.与人白细胞介素-4基因调控性P序列(5'-CGAAAATTTCC-3')相互作用的核因子NF(P)的特性:与核因子κB和活化T细胞核因子的关系
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8
Involvement of the cyclic AMP-responsive element binding protein in bovine leukemia virus expression in vivo.环磷酸腺苷反应元件结合蛋白参与牛白血病病毒的体内表达。
J Virol. 1994 Sep;68(9):5845-53. doi: 10.1128/JVI.68.9.5845-5853.1994.
9
Function and activation of NF-kappa B in the immune system.免疫系统中核因子-κB的功能与激活
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10
Enhanced B-lymphocyte expression of IL-2R alpha associated with T lymphocytosis in BLV-infected persistently lymphocytotic cows.在感染牛白血病病毒(BLV)且持续淋巴细胞增多的奶牛中,白细胞介素-2受体α(IL-2Rα)的B淋巴细胞表达增强与T淋巴细胞增多相关。
Leukemia. 1994 Jun;8(6):1057-61.

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.

DOI:10.1128/JVI.69.10.6005-6009.1995
PMID:7666505
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC189496/
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。