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作 者:孙鹏[1,2] 宋娟[2] 张瑾[2] 宋芹芹[2] 甘星[2] 崔雨[2] 高晨[2] 博晓真[1] 韩俊[2]
机构地区:[1]内蒙古医学院微生物教研室,呼和浩特010110 [2]中国疾病预防控制中心病毒病预防控制所传染病预防控制国家重点实验室,北京100052
出 处:《病毒学报》2012年第4期414-417,共4页Chinese Journal of Virology
基 金:传染病重大专项(2009ZX10004-101;2008ZX10004-002);重点实验室发展基金(2008SKLID102;2011SKLID104)资助
摘 要:本研究将PrP106-126多肽和HeLa细胞共孵育4h和8h,采用Hoechst染色分析发现PrP106-126诱导凋亡细胞细胞核出现不同程度的染色质浓集,固缩及碎裂的细胞凋亡征象。Western blotting检测发现PrP106-126诱导细胞中的多聚ADP核糖聚合酶(poly ADP-ribose polymerase,PARP)降解,提示PrP106-126通过caspase3途径引起细胞凋亡现象。PrP106-126诱导的细胞中14-3-3β在不同孵育时间也出现降解,而Real-time PCR检测14-3-3βmRNA未发生变化。本研究证明PrP106-126通过caspase3诱导HeLa细胞凋亡,并可导致抗凋亡蛋白14-3-3β的降解而加速凋亡的形成。To investigate changes of 14-3-3β from apoptosis induced by PrP106-126 polypeptide, H eLa cell was incubated with PrP106-126 for 4h or 8h. Nucleus changes and the expression of PARP were detected differently by Hoechst staining and Western blotting. Expressing of protein and mRNA from 14-3-3β was determined by Western blotting and Real-time PCR. The results show that typical nucleus pyknosis and chip of apoptosis and degradation of PARP were induced by PrP106-126 peptide in HeLa cells. Degradation of 14-3-3β appeared in apoptosis groups induced by PrP106-126 peptide. However, 14-3-3β mRNA did not display any changes in apoptosis groups. This study indicated that degradation of antiapoptosis protein 14- 3-3β induced by PrP106-126 peptide may be one of pathogenesis mechanism of prion disease.
关 键 词:PrP106-126 凋亡 14-3-3β
分 类 号:R373.9[医药卫生—病原生物学]
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