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Transcriptional regulation of the human papillomavirus-16 E6-E7 promoter by a keratinocyte-dependent enhancer, and by viral E2 trans-activator and repressor gene products: implications for cervical carcinogenesis 总被引:53,自引:4,他引:49 下载免费PDF全文
T P Cripe T H Haugen J P Turk F Tabatabai P G Schmid rd M Dürst L Gissmann A Roman L P Turek 《The EMBO journal》1987,6(12):3745-3753
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Transcriptional enhancer factor (TEF)-1 and its cell-specific co-activator activate human papillomavirus-16 E6 and E7 oncogene transcription in keratinocytes and cervical carcinoma cells. 总被引:4,自引:0,他引:4 下载免费PDF全文
T Ishiji M J Lace S Parkkinen R D Anderson T H Haugen T P Cripe J H Xiao I Davidson P Chambon L P Turek 《The EMBO journal》1992,11(6):2271-2281
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The enhancer in the long control region of human papillomavirus type 16 is up-regulated by PEF-1 and down-regulated by Oct-1. 总被引:3,自引:1,他引:2 下载免费PDF全文
The minimal enhancer in the long control region of human papillomavirus type 16 regulates cell type and constitutive expression from the promoter P97. This region contains at least four DNase I footprints (fp4e, fp5e, fp6e, and fp7e). We have shown that fp5e is crucial to enhancer function and have described an apparently novel factor (PEF-1) binding fp5e (S. Cuthill, G. J. Sibbet, and M. S. Campo, Mol. Carcinog. 8:9-104, 1993). Further analyses reveal that Oct-1 or an Oct-related factor binds fp5e at a site overlapping that of PEF-1. The binding of Oct-1 to fp5e has been demonstrated by electrophoretic mobility shift assays, by oligonucleotide competition studies, and by using an Oct-1-specific anti-POU serum. The location of the Oct-1 site has been confirmed by a panel of mutants across fp5e. Mutations that block PEF-1 binding to fp5e also block enhancer/promoter activity of the long control region, whereas mutations that block Oct-1 binding significantly increase enhancer/promoter activity. Thus, although both PEF-1 and Oct-1 interact with fp5e, they appear to regulate human papillomavirus expression in opposite ways. 相似文献
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细胞转录调节因子 Y Y1 可抑制人乳头瘤病毒16 型( H P V 16) 癌基因启动子 P97 的活性, Y Y1 位点的突变和缺失不仅可诱导 P97 活性增强而且可在全基因组内增强 E6 癌基因转录,同时使病毒对啮齿类动物纤维细胞的转化能力增强。为了观测人乳头瘤病毒16 型长控制区( H P V16 L C R) 序列上 Y Y1 蛋白特异性结合位点破坏在完整基因组范围内对人原代包皮角源细胞永生化能力的影响,将 H P V 16 Y Y1 位点突变株和野毒株转染至人原代包皮角源细胞。筛选结果表明,突变株可诱导形成永生化细胞,永生化能力明显高于野毒株。对4 株永生化细胞系 D N A检测发现,均含有呈整合状态的 H P V 16 D N A,其中3 株的 E1/ E2 区域有缺失。 R N A 检测显示,4株细胞内均有 E6/ E7 m R N A 的转录。这表明, H P V 16 L C R 上 Y Y1 蛋白特异性结合位点的破坏,可在完整基因组范围内增强病毒使人原代包皮角源细胞永生化的能力。 相似文献
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Transcriptional activation of the human papillomavirus-16 P97 promoter by an 88-nucleotide enhancer containing distinct cell-dependent and AP-1-responsive modules 总被引:17,自引:0,他引:17
T P Cripe A Alderborn R D Anderson S Parkkinen P Bergman T H Haugen U Pettersson L P Turek 《The New biologist》1990,2(5):450-463
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