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作 者:杨海宁[1] 于修平[2] 卞继峰[2] JasonJChen 赵蔚明[1] 贾继辉[1] 周亚滨[1] 刘颖[1] 栾怡[1] 齐眉[1]
机构地区:[1]山东大学医学院微生物学教研室,济南250012 [2]山东大学医学院分子生物学实验室,济南250012 [3]DepartmentofMedicine,UMassMedicalSchool
出 处:《基础医学与临床》2002年第4期346-350,共5页Basic and Clinical Medicine
基 金:国家自然科学基金 (39870 739)
摘 要:通过PCR方法从人乳头瘤病毒 5 8型 (HPV5 8)全基因克隆中扩增出HPV5 8E6基因片段 ,克隆至真核表达质粒pcDNA3的T7启动子下游 ,并在体外转录成mRNA后 ,在源自网织红细胞的翻译缓冲液中成功表达了含有生物素标记的HPV5 8E6蛋白 ,并在体外成功发现HPV5 8E6能够降解p5 3蛋白 ,从而推断结合并降解p5 3蛋白是其致癌作用的关键环节 。Human papillomavirus type 58 (HPV58) is prevalent in cervical carcinomas among Chinese women but the mechanism by which HPV58 induces squamous cell carcinomas is not known. As an initial step to understand the molecular basis of HPV58 associated malignancies, the DNA fragment encoding HPV58 E6 was amplified from HPV58 genome by PCR and cloned into the expression vector pcDNA3. The recombinant plasmid was transcripted in vitro and then translated into biotin labeled HPV58 E6 protein in rabbit reticulocyte lysate. The in vitro interaction of HPV58 E6 and p53 protein was then investigated. Significantly, our result demonstrates that HPV58 E6 promotes the degradation of p53. Our data suggest that the ability of HPV58 E6 to inactivate p53 is a mechanism by which the viral protein induces tumors.
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