Residential College | false |
Status | 已發表Published |
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 Publication | APOPTOSIS |
ISSN | 1360-8185 |
Volume | 23Issue: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. |
Keyword | Mlkl Eif2α Ros Apoptosis Chelerythrine |
DOI | 10.1007/s10495-018-1475-6 |
Indexed By | SCIE |
Language | 英語English |
WOS Research Area | Biochemistry & Molecular Biology ; Cell Biology |
WOS Subject | Biochemistry & Molecular Biology ; Cell Biology |
WOS ID | WOS:000446064700006 |
Publisher | SPRINGER, VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS |
Scopus ID | 2-s2.0-85051186256 |
Fulltext Access | |
Citation statistics | |
Document Type | Journal article |
Collection | Institute of Chinese Medical Sciences |
Corresponding Author | Jin‑Jian Lu |
Affiliation | State 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 Affilication | Institute of Chinese Medical Sciences |
Corresponding Author Affilication | Institute of Chinese Medical Sciences |
Recommended Citation 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., Xia Guo., Min‑Xia Su., Xiuping Chen., & 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. |
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