BAX Inhibitor-1 Is a Negative Regulator of the ER Stress Sensor IRE1α

被引:277
作者
Lisbona, Fernanda [7 ]
Rojas-Rivera, Diego [7 ]
Thielen, Peter [1 ]
Zamorano, Sebastian [7 ]
Todd, Derrick [1 ,2 ]
Martinon, Fabio [1 ]
Glavic, Alvaro [6 ]
Kress, Christina [3 ]
Lin, Jonathan H. [4 ,5 ]
Walter, Peter [4 ,5 ]
Reed, John C. [3 ]
Glimcher, Laurie H. [1 ,2 ]
Hetz, Claudio [1 ,7 ]
机构
[1] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA
[2] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA
[3] Burnham Inst Med Res, La Jolla, CA 92037 USA
[4] Univ Calif San Francisco, Dept Biochem & Biophys, San Francisco, CA 94158 USA
[5] Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94158 USA
[6] Univ Chile, Dept Biol, Ctr Genom Cell, Fac Sci, Santiago, Chile
[7] Univ Chile, Inst Biomed Sci, FONDAP Ctr Mol Studies Cell, Santiago, Chile
基金
美国国家卫生研究院;
关键词
UNFOLDED PROTEIN RESPONSE; ENDOPLASMIC-RETICULUM STRESS; BCL-X-L; PLASMA-CELL DIFFERENTIATION; TRANSCRIPTION FACTOR; XBP-1; FAMILY; GENE; BIOGENESIS; SUPPRESSOR;
D O I
10.1016/j.molcel.2009.02.017
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Adaptation to endoplasmic reticulum (ER) stress depends on the activation of an integrated signal transduction pathway known as the unfolded protein response (UPR). Bax inhibitor-1 (BI-1) is an evolutionarily conserved ER-resident protein that suppresses cell death. Here we have investigated the role of BI-1 in the UPR. BI-1 expression suppressed IRE1 alpha activity in fly and mouse models of ER stress. BI-1-deficient cells displayed hyperactivation of the ER stress sensor IRE1 alpha, leading to increased levels of its downstream target X-box-binding protein-1 (XBP-1) and upregulation of UPR target genes. This phenotype was associated with the formation of a stable protein complex between BI-1 and IRE1 alpha, decreasing its ribonuclease activity. Finally, BI-1 deficiency increased the secretory activity of primary B cells, a phenomenon regulated by XBP-1. Our results suggest a role for BI-1 in early adaptive responses against ER stress that contrasts with its known downstream function in apoptosis.
引用
收藏
页码:679 / 691
页数:13
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