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	TRIM25 protects tumor cells from ER stress induced apoptosis through regulating Keap1-Nrf2 pathway
	Guixin Zhu; Yi Xu; Junlin Teng; Jianguo Chen; Liang Chen.
	2018
会议日期	2018
英文摘要	Endoplasmic reticulum (ER) quality control is crucial for ER and cellular protein homeostasis while its dysregulation is related to cancer and other diseases. Here, we screened all of the tripartite motif (TRIM) family members, which are closely linked to protein quality control, and identified that TRIM25 enhances ER protein quality control and inhibits ER stress induced apoptosis. We show that depletion of TRIM25 activates the UPR signaling pathway, especially through the activation of c-Jun N-terminal kinase, and inhibits ER-associated protein degradation. In addition, TRIM25 reduces the protein level of Keap1 through ubiquitination, which activates Nrf2 by promoting its nuclear import, resulting in decreased cellular ROS levels and protection of cells from apoptosis during ER stress. Moreover, the expression level of TRIM25 is up-regulated in breast tumors, and high levels of TRIM25 correlate with poor clinical survival. These findings reveal that TRIM25, a novel regulator of ER quality control, suppresses ER stress induced ROS and apoptosis by elevating levels of activated Nrf2 in the nucleus.
语种	中文
内容类型	会议论文
源URL	[http://ir.siat.ac.cn:8080/handle/172644/14754]
专题	深圳先进技术研究院_医药所
推荐引用方式 GB/T 7714	Guixin Zhu,Yi Xu,Junlin Teng,et al. TRIM25 protects tumor cells from ER stress induced apoptosis through regulating Keap1-Nrf2 pathway[C]. 见:. 2018.

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