Human macrophage inflammatory protein-3α/CCL20/LARC/Exodus/SCYA20 is transcriptionally upregulated by tumor necrosis factor-α via a non-standard NF-κB site
Human macrophage inflammatory protein-3α/CCL20/LARC/Exodus/SCYA20 is transcriptionally upregulated by tumor necrosis factor-α via a non-standard NF-κB site
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DOI：
10.1016/s0014-5793(01)03138-6
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发表时间：
2001-12-14
期刊：
影响因子：
3.5
通讯作者：
Lindley, IJD
中科院分区：
文献类型：
--
作者：
Harant, H;Eldershaw, SA;Lindley, IJD
克隆人巨噬细胞炎性蛋白-3 α/CCL 20基因的5 ′-侧翼序列，并在荧光素酶报告基因构建体中转染到G-361人黑素瘤细胞中。肿瘤坏死因子-α（TNF-α）处理刺激荧光素酶表达，启动子截短表明，TNF-α诱导是由nt-111和-77之间的区域赋予的，该区域含有非标准的核因子-κ B（NT-κ B）结合位点。对NT-κ B的需要被证明如下：（i）该NF-κ B位点的突变消除了TNF-α的反应性;（ii）TNF-α激活了含有两个拷贝的CCL 20 NF-κ B结合位点的构建体;（iii）NF-κ B p65的过表达激活了CCL 20启动子;（iv）来自TNF-α刺激的细胞的核提取物的NF-κ B特异性地结合到该NF-κ B位点。(C)2001年欧洲生物化学学会联合会。由Elsevier Science B. V.出版，版权所有。
The 5'-flanking sequences of the human macrophage inflammatory protein-3 alpha /CCL20 gene were cloned and transfected into G-361 human melanoma cells in a luciferase reporter construct. Tumor necrosis factor-alpha (TNF-alpha) treatment stimulated luciferase expression, and promoter truncations demonstrated that TNT-alpha inducibility is conferred by a region between nt -111 and -77, which contains a non-standard nuclear factor-kappaB (NT-kappaB) binding site. The requirement for NT-kappaB was demonstrated as follows: (i) mutations in this NF-kappaB site abrogated TNF-alpha responsiveness; (ii) TNF-a activated a construct containing two copies of the CCL20 NF-kappaB binding site; (iii) overexpression of NF-kappaB p65 activated the CCL20 promoter; (iv) NF-kappaB from nuclear extracts of TNF-alpha -stimulated cells bound specifically to this NF-kappaB site. (C) 2001 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.