UM  > 中華醫藥研究院
MLKL mediates apoptosis via a mutual regulation with PERK/eIF2 alpha pathway in response to reactive oxygen species generation
Wen‑Xiang Cao; Ting Li; Zheng‑Hai Tang; Le‑Le Zhang; Zhao‑Yu Wang; Xia Guo; Min‑Xia Su; Xiuping Chen; Jin‑Jian Lu
2018-08-06
Source PublicationAPOPTOSIS
ISSN1360-8185
Volume23Issue:9-10Pages:521-531
Abstract

The pseudokinase mixed lineage kinase domain-like protein (MLKL) is a core effector of necroptosis, and its function in necroptosis is widely studied. However, the function of MLKL in apoptosis remains unclear. In the present study, the role of MLKL in chelerythrine (CHE)-promoted apoptosis was studied. A special band of MLKL (i.e., *MLKL) was observed after treatment with CHE. MLKL and *MLKL were accumulated in the nucleus upon treatment with CHE and MLKL silencing reversed the CHE-induced apoptosis. Blockade of CHE-triggered reactive oxygen species (ROS) generation or inhibition of CHE-activated protein kinase-like endoplasmic reticulum kinase (PERK)-eukaryotic initiation factor 2 α subunit (eIF2α) pathway reversed the apoptosis. A decreased ROS level inhibited CHE-mediated nuclear translocation of MLKL and *MLKL and the activation of eIF2α, whereas MLKL or eIF2α silencing did not affect the CHE-triggered ROS generation. Furthermore, MLKL silencing prevented the CHE-activated eIF2α signal, and eIF2α silencing blocked the CHE-induced nuclear translocation of MLKL and *MLKL. Our studies suggested that CHE possibly induces apoptosis through the nuclear translocation of MLKL and *MLKL, which is promoted by a mutual regulation between MLKL and PERK–eIF2α pathway in response to ROS formation. The present study clarified the new function of MLKL in apoptosis.

KeywordMlkl Eif2α Ros Apoptosis Chelerythrine
DOI10.1007/s10495-018-1475-6
Indexed BySCI
Language英语
WOS Research AreaBiochemistry & Molecular Biology ; Cell Biology
WOS SubjectBiochemistry & Molecular Biology ; Cell Biology
WOS IDWOS:000446064700006
PublisherSPRINGER, VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
全文获取链接
引用统计
Document TypeJournal article
专题Institute of Chinese Medical Sciences
Corresponding AuthorJin‑Jian Lu
AffiliationState Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, 7014, N22, Avenida da Universidade, Taipa, Macao, China
First Author AffilicationInstitute of Chinese Medical Sciences
Corresponding Author AffilicationInstitute of Chinese Medical Sciences
推荐引用方式
GB/T 7714
Wen‑Xiang Cao,Ting Li,Zheng‑Hai Tang,et al. MLKL mediates apoptosis via a mutual regulation with PERK/eIF2 alpha pathway in response to reactive oxygen species generation[J]. APOPTOSIS,2018,23(9-10):521-531.
APA Wen‑Xiang Cao.,Ting Li.,Zheng‑Hai Tang.,Le‑Le Zhang.,Zhao‑Yu Wang.,...&Jin‑Jian Lu.(2018).MLKL mediates apoptosis via a mutual regulation with PERK/eIF2 alpha pathway in response to reactive oxygen species generation.APOPTOSIS,23(9-10),521-531.
MLA Wen‑Xiang Cao,et al."MLKL mediates apoptosis via a mutual regulation with PERK/eIF2 alpha pathway in response to reactive oxygen species generation".APOPTOSIS 23.9-10(2018):521-531.
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
Google Scholar
中相似的文章 Google Scholar
[Wen‑Xiang Cao]的文章
[Ting Li]的文章
[Zheng‑Hai Tang]的文章
Baidu academic
中相似的文章 Baidu academic
[Wen‑Xiang Cao]的文章
[Ting Li]的文章
[Zheng‑Hai Tang]的文章
Bing Scholar
中相似的文章 Bing Scholar
[Wen‑Xiang Cao]的文章
[Ting Li]的文章
[Zheng‑Hai Tang]的文章
相关权益政策
暂无数据
收藏/分享
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。