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作 者:董小平[1,2] 刘红[1,2] HerbertPfister
机构地区:[1]中国预防医学科学院病毒学研究所 [2]首都医科大学附属口腔医院
出 处:《病毒学报》1999年第2期125-129,共5页Chinese Journal of Virology
摘 要:人乳头瘤病毒16型(HPV16)癌基因的表达受病毒早期启动子P97的控制。位于LCR上YY1蛋白结合位点的破坏可明显提高P97的活性。为了观测YY1位点破坏在全基因组范围内对病毒e6/e7基因转录的影响,将构建的带有LCR特异性突变的重组HPV16全基因组DNA和HPV16野毒株DNA转染至培养细胞,同时组建HPV16E6反向序列RNA体外转录质粒。RNase保护试验证实,突变HPV16DNA在短暂转染细胞中可诱导更多量的E6特异性mRNA转录。这一结果提示,LCR上YY1位点的破坏可促进HPV16癌基因的转录,从而使感染细胞具有更高的癌变可能性。The expression of viral oncogenes of HPV 16 is controlled by the early promoter P97. Removal of YY1 binding sites in the long control regcon(LCR) can increase the activity of P97 in transient transfection assays. To analyse the effect on the transcription of viral oncogenes, due to destroying YY1's repression, we transfected HT3 cells separately with newly constructed HPV 16 DNAs containing mutated LCRs and the HPV 16 wild-type DNA. Meanwhile a subfragment of HPV 16 E6 antisense RNA was transcribed in vitro according to a newly generated plasmid. RNase protection assay showed that more E6 specific mRNAs could be detected under the control of the mutated HPV 16 DNAs. It suggests that removal of YY1 binding sequences in the LCR improves the transcription of viral oncogenens, thereby, might increase the viral oncogenicity.
分 类 号:R373.9[医药卫生—病原生物学] R730.2[医药卫生—基础医学]
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