TRANSCRIPTION OF THE TRANSFORMING GENES OF THE ONCOGENIC HUMAN PAPILLOMAVIRUS-16 IS STIMULATED BY TUMOR PROMOTORS THROUGH AP1 BINDING-SITES
TRANSCRIPTION OF THE TRANSFORMING GENES OF THE ONCOGENIC HUMAN PAPILLOMAVIRUS-16 IS STIMULATED BY TUMOR PROMOTORS THROUGH AP1 BINDING-SITES
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DOI：
10.1093/nar/18.4.763
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发表时间：
1990-02-25
影响因子：
14.9
通讯作者：
KLOCK, G
中科院分区：
文献类型：
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作者：
CHAN, WK;CHONG, T;KLOCK, G
人乳头瘤病毒 16 (HPV-16) 的启动子 P97 产生编码病毒主要转化基因 E6 和 E7 的转录本。 P97 的活性受细胞类型特异性增强剂以及糖皮质激素和黄体酮的调节。我们在此表明，在含有 HPV-16 基因组的 CaSki 细胞中，P97 也可由佛波酯诱导。对病毒增强子的限制性片段和寡核苷酸的功能分析将两个佛波酯反应元件定位在两个转录因子结合位点（称为 fp4e 和 fp9e）上。克隆基序的序列比较、足迹分析和带移竞争表明 fp4e 和 fp9e 均与转录因子 AP1 结合。 HPV-16 和其他乳头瘤病毒中的这些 AP1 结合位点可能提供细胞癌基因（如 jun、fos 和可能的 ras）之间的联系，其转录刺激活性可能导致病毒转化基因 E6 和 E7 的表达升高。
The promoter P97 of human papillomavirus-16 (HPV-16) gives rise to transcripts that encode the principal transforming genes of the virus, E6 and E7. The activity of P97 is regulated by a cell-type-specific enhancer, as well as by glucocorticoids and progesterone. We show here, that in CaSki cells, which contain HPV-16 genomes, P97 is also inducible by phorbol esters. Functional analysis of restriction fragments and oligonucleotides of the viral enhancer localizes two phorbol ester response elements on two transcription factor binding sites termed fp4e and fp9e. Sequence comparison, footprint analysis and bandshift competition of the cloned motifs suggest that both fp4e and fp9e are bound by the transcription factor AP1. These AP1 binding sites in HPV-16 and other papillomaviruses may provide a link between cellular oncogenes like jun, fos and possibly ras, whose transcription stimulating activity may lead to an elevated expression of the viral transforming genes E6 and E7.