共 47 条
BAX Inhibitor-1 Is a Negative Regulator of the ER Stress Sensor IRE1α
被引:277
作者:

Lisbona, Fernanda
论文数: 0 引用数: 0
h-index: 0
机构:
Univ Chile, Inst Biomed Sci, FONDAP Ctr Mol Studies Cell, Santiago, Chile Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA

Rojas-Rivera, Diego
论文数: 0 引用数: 0
h-index: 0
机构:
Univ Chile, Inst Biomed Sci, FONDAP Ctr Mol Studies Cell, Santiago, Chile Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA

Thielen, Peter
论文数: 0 引用数: 0
h-index: 0
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Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA

Zamorano, Sebastian
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h-index: 0
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Univ Chile, Inst Biomed Sci, FONDAP Ctr Mol Studies Cell, Santiago, Chile Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA

Todd, Derrick
论文数: 0 引用数: 0
h-index: 0
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Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA
Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA

Martinon, Fabio
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h-index: 0
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Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA

Glavic, Alvaro
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h-index: 0
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Univ Chile, Dept Biol, Ctr Genom Cell, Fac Sci, Santiago, Chile Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA

Kress, Christina
论文数: 0 引用数: 0
h-index: 0
机构:
Burnham Inst Med Res, La Jolla, CA 92037 USA Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA

Lin, Jonathan H.
论文数: 0 引用数: 0
h-index: 0
机构:
Univ Calif San Francisco, Dept Biochem & Biophys, San Francisco, CA 94158 USA
Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94158 USA Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA

Walter, Peter
论文数: 0 引用数: 0
h-index: 0
机构:
Univ Calif San Francisco, Dept Biochem & Biophys, San Francisco, CA 94158 USA
Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94158 USA Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA

Reed, John C.
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h-index: 0
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Burnham Inst Med Res, La Jolla, CA 92037 USA Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA

Glimcher, Laurie H.
论文数: 0 引用数: 0
h-index: 0
机构:
Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA
Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA

Hetz, Claudio
论文数: 0 引用数: 0
h-index: 0
机构:
Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA
Univ Chile, Inst Biomed Sci, FONDAP Ctr Mol Studies Cell, Santiago, Chile Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA
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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