Journal
CELL CYCLE
Volume 11, Issue 6, Pages 1118-1122Publisher
LANDES BIOSCIENCE
DOI: 10.4161/cc.11.6.19529
Keywords
ER stress; SENP1; SUMO; XBP1
Categories
Funding
- National Natural Science Foundation of China [30900740, 81071665, 91019021]
- National Basic Research Program of China (973 Program) [2010CB912104]
- Shanghai Committee of Science and Technology [1014090200, 10410700900, 11XD1403200, 11DZ2260200]
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The transcription factor X box-binding protein 1 (XBP1) is a key component of the endoplasmic reticulum (ER) stress response. Recently, it has been reported that the spliced XBP1 (XBP1s), an activated XBP1 during ER stress, can be SUMOylated. Here, we identify Sentrin/SUMO-specific protease 1 (SENP1) as a specific de-SUMOylation protease for XBP1. SENP1 can increase the transcriptional activity of XBP1. In Senp1(-/-) cells, the SUMOylated XBP1 is accumulated, and the expression of XBP1 target genes is downregulated in response to ER stress. Moreover, SENP1 deficiency significantly increases ER stress-induced apoptosis through accumulating XBP1 SUMOylation. These results reveal an essential function of SENP1 in ER stress response through regulating XBP1 SUMOylation.
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