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Coxsackievirus B3-induced apoptosis and Caspase-3

Coxsackievirus B3-induced apoptosis and Caspase-3

作     者:JIAN PING YUAN,WEI ZHAO,HONG TAO WANG,KAI Yu WU,TAO LI,XIAO KUI GUO,SHAN QING TONGDepartment of Microbiology and Parasitology,Shanghai Second Medical University,Shanghai 200025,China 

作者机构:Department of Microbiology and Parasitology Shanghai Second Medical University Shanghai China 

出 版 物:《Cell Research》 (细胞研究(英文版))

年 卷 期:2003年第13卷第3期

页      面:203-209页

核心收录:

学科分类:1007[医学-药学(可授医学、理学学位)] 100705[医学-微生物与生化药学] 1001[医学-基础医学(可授医学、理学学位)] 100103[医学-病原生物学] 10[医学] 

主  题:Coxsackievirus B3 (CVB3) apoptosis. caspase-3. 

摘      要:Cell death can be classified into two categories: apoptosis and necrosis. Apoptotic pathway can beeither caspase-dependent or caspase-independent. Caspase-independent cytopathic effect (CPE) has beendescribed. In order to evaluate the pattern of HeLa cell death induced by Coxsackievirus B3 (CVB3)and whether apoptosis involves caspase activation, we co-cultivated HeLa cells with CVB3 and detectedthe cytopathic changes, the alteration of mRNA and protein expression of caspase-3 gene plus caspase-3activity, as well as analyzing DNA fragmentation before and after caspase-3 activity inhibition. Accordingto the results, we propose that CVB3 may induce apoptosis and necrosis in HeLa cells, the latter appearingmuch earlier. Caspase-3 is activated at the levels of both transcription and translation, and procaspase-3 isproteolytically cleaved, thus leading to the continuous increasing of both caspase-3 precursor protein and itssubunit. However, besides CPE, apoptosis induced by CVB3 is not a direct consequence of

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