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学科主题临床医学
PARP and RIP-1 are required for autophagy induced by 11 ′-deoxyverticillin A, which precedes caspase-dependent apoptosis
Zhang, Nan6; Chen, Yali1; Jiang, Ruixuan4; Li, Erwei1; Chen, Xiuling2; Xi, Zhijun6; Guo, Yinglu6; Liu, Xingzhong1; Zhou, Yuguang2,3; Che, Yongsheng1,5; Jiang, Xuejun1,2
关键词11 &prime -deoxyverticillin A autophagy apoptosis PARP RIP
刊名AUTOPHAGY
2011-06-01
DOI10.4161/auto.7.6.15103
7期:6页:598-612
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Cell Biology
资助者National Natural Science Foundation of China (NSFC) ; Ministry of Science and Technology of China ; National Natural Science Foundation of China (NSFC) ; Ministry of Science and Technology of China
研究领域[WOS]Cell Biology
关键词[WOS]NECROTIC CELL-DEATH ; POLY(ADP-RIBOSE) POLYMERASE-1 ; MONITORING AUTOPHAGY ; MEDIATED CLEAVAGE ; REDOX REGULATION ; SELF-DIGESTION ; DNA-DAMAGE ; HELA-CELLS ; SURVIVAL ; DEGRADATION
英文摘要

The epipolythiodioxopiperazines (ETPs) are fungal secondary metabolites proven to trigger both apoptotic and necrotic cell death of tumor cells. However, the underlying mechanism of their regulatory role in macroautophagy and the interplay between autophagy and apoptosis initiated by the ETPs, remain unexplored. In the current work, we found that 11′-deoxyverticillin A (C42), a member of the ETPs, induces autophagosome formation, accumulation of microtubule-associated protein 1 light chain 3-II (LC3-II) and degradation of sequestosome 1 (SQSTM1/p62). In addition, the LC3-II accrual and p62 degradation occur prior to caspase activation and coincide with PARP activation. Inhibition of autophagy by either chemical inhibitors or by RNA interference single knockdown of essential autophagic genes partially reduces the cell death and the cleavage of both caspase 3 and PARP. Necrostatin-1, a specific inhibitor of necroptosis, inhibits both the augmentation of LC3-II and the cleavage of caspase 3, which was confirmed by depletion of receptor-interacting protein 1 (RIP-1), a crucial necrostatin-1-targeted adaptor kinase mediating cell death and survival. Moreover, inhibition of PARP by either chemical inhibitors or RNA interference provides obvious protection for cell viability and suppresses the LC3-II accretion caused by C42 treatment. Interestingly, double silencing of LC3 and p62 completely suppressed PARP cleavage and concurrently and maximally augmented the PAR formation induced by C42. Collectively, we have demonstrated that C42 enhances the cellular autophagic process, which requires both PARP and RIP-1 participation, preceding and possibly augmenting, the caspase-dependent apoptotic cell death.

语种英语
所属项目编号90408024 ; 30900731 ; 30672097 ; 30870057 ; 30925039 ; 2009CB522302 ; 2009ZX09302-004
资助者National Natural Science Foundation of China (NSFC) ; Ministry of Science and Technology of China ; National Natural Science Foundation of China (NSFC) ; Ministry of Science and Technology of China
WOS记录号WOS:000291153300005
引用统计
被引频次:63[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/61867
专题北京大学第一临床医学院_泌尿外科
作者单位1.Chinese Acad Sci, Key Lab Systemat Mycol & Lichenol, Beijing, Peoples R China
2.Chinese Acad Sci, Biol Resource Ctr, Beijing, Peoples R China
3.Chinese Acad Sci, Inst Microbiol, State Key Lab Microbial Resources, Beijing, Peoples R China
4.Capital Med Univ, Beijing, Peoples R China
5.Beijing Inst Pharmacol & Toxicol, Beijing, Peoples R China
6.Peking Univ, Hosp 1, Inst Urol, Natl Res Ctr Urol Canc, Beijing 100871, Peoples R China
推荐引用方式
GB/T 7714
Zhang, Nan,Chen, Yali,Jiang, Ruixuan,et al. PARP and RIP-1 are required for autophagy induced by 11 ′-deoxyverticillin A, which precedes caspase-dependent apoptosis[J]. AUTOPHAGY,2011,7(6):598-612.
APA Zhang, Nan.,Chen, Yali.,Jiang, Ruixuan.,Li, Erwei.,Chen, Xiuling.,...&Jiang, Xuejun.(2011).PARP and RIP-1 are required for autophagy induced by 11 ′-deoxyverticillin A, which precedes caspase-dependent apoptosis.AUTOPHAGY,7(6),598-612.
MLA Zhang, Nan,et al."PARP and RIP-1 are required for autophagy induced by 11 ′-deoxyverticillin A, which precedes caspase-dependent apoptosis".AUTOPHAGY 7.6(2011):598-612.
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