牛乳头瘤病毒E6蛋白与p73蛋白的相互作用  

Interaction of bovine papillomavirus E6 protein with p73

作　　者：杨海宁[1] 于修平[2] Yi hui Hong Minjie Du JasonJ. Chen 卞继峰[2] 赵蔚明[1] 

机构地区：[1]山东大学医学院微生物学教研室 [2]山东大学医学院分子生物学实验室 [3]Department of Dermatology,Tufts Univeristy and New England Medical Center,750 WashingtonSt,Box166,Boston,MA02111

出　　处：《基础医学与临床》2002年第2期138-142,共5页Basic and Clinical Medicine

基　　金：国家自然科学基金 (39870 739)

摘　　要：为进一步探讨和阐明E6蛋白的致癌机制以及充分认识新发现的抑癌基因p73的作用 ,在体外通过免疫共沉淀法研究p73和牛乳头瘤病毒 1型E6蛋白 (BPV 1E6 )的相互结合情况 ,后将表达p73和BPV 1E6的质粒导入SAOS 2细胞内 ,进一步研究细胞内E6蛋白对p73蛋白的诱导凋亡和转录活化功能等生物学活性的影响。结果发现 ,BPV 1E6与p73蛋白结合较弱 ,且未检测到E6能诱导p73蛋白的降解。在SAOS 2细胞内 ,BPV 1E6蛋白确实能部分抑制p73蛋白的诱导细胞凋亡的功能 ,并且E6蛋白对p73蛋白的转录激活作用也有影响 ,但这种影响作用颇弱。To explore the carcinogenic machanism of E6 and the function of p73, a newly discovered tumor suppressor, the binding of the in vitro-translated p73 and BPV-1 E6 proteins was investigated by coimmunoprecipitation. Then the p73 and BPV-1 E6 expression plasmids were cotransfected into SAOS-2 cells and the effect of E6 on p73's biological functions such as cell apoptosis and transcriptional activation was analysed. The result showed that the binding of BPV-1 E6 and p73 proteins was weak and p73 degradation promoted by E6 was not detectable. In SAOS-2 cells, BPV-1 E6 protein inhibited p73-induced apoptosis and transactivation though the effect was weak.

关 键 词：乳头瘤病毒 E6蛋白 P73蛋白 致癌机制 免疫共泡淀法 

分 类 号：R730.2[医药卫生—肿瘤]