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- W3150900830 abstract "细胞信号转导异常可揭示人类疾病发生的本质, 一些病毒的致病机制即源于其蛋白所致宿主细胞内信号转导的紊乱. 丙型肝炎病毒(HCV)感染是引起人类严重肝脏疾病的主要病因, 但致病机制尚未明确. HCV包膜蛋白2(E2蛋白)能介导病毒吸附并结合至靶细胞表面, 此乃HCV感染的前提及首发事件. 推测HCV E2蛋白经与其受体(人CD81)的相互作用而将病毒感染信号传递至宿主细胞内, 使细胞增殖和分化异常, 从而导致感染细胞发生早期病变. 为进一步验证此致病机制, 研究了HCV E2蛋白等诸因素对差异表达人CD81的U937, Molt-4细胞内MAPK/ERK途径的影响, 结果表明, HCV E2蛋白可特异性激活细胞内MAPK/ERK途径, 而HCV E2单抗、CD81单抗、 慢性HCV感染患者血清或MAPK/ERK途径上游MEK1的抑制剂(PD98059)均不同程度地减弱或抑制HCV E2蛋白对MAPK/ERK的激活. 此外, PD98059尚可抑制HCV E2蛋白对MAPK/ERK途径下游转录因子Elk-1的活化. 研究认为, HCV E2蛋白经其相应受体引发的宿主细胞跨膜信号转导异常很可能是HCV的致病机制之一." @default.
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- W3150900830 date "2003-01-01" @default.
- W3150900830 modified "2023-10-16" @default.
- W3150900830 title "丙型肝炎病毒致病新模式: 包膜蛋白2对MAPK/ERK途径的激活" @default.
- W3150900830 doi "https://doi.org/10.1360/zc2003-33-3-246" @default.
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