BAX Inhibitor-1 Is a Negative Regulator of the ER Stress Sensor IRE1 alpha

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BAX Inhibitor-1 Is a Negative Regulator of the ER Stress Sensor IRE1 alpha

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BAX Inhibitor-1 Is a Negative Regulator of the ER Stress Sensor IRE1 alpha

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Título: BAX Inhibitor-1 Is a Negative Regulator of the ER Stress Sensor IRE1 alpha
Autor: Lisbona, Fernanda; Rojas Rivera, Diego; Thielen, Peter; Zamorano, Sebastián; Todd, Derrick; Martinon, Fabio; Glavic, Alvaro; Kress, Christina; Lin, Jonathan H.; Walter, Peter; Reed, John C.; Glimcher, Laurie H.; Hetz, Claudio
Resumen: 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 IRE1α activity in fly and mouse models of ER stress. BI-1 deficient cells displayed hyperactivation of the ER stress sensor IRE1α, 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 IRE1α, 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 new role for BI-1 in early adaptive responses against ER stress which contrasts with its known downstream function in apoptosis.
URI: http://www.captura.uchile.cl/handle/2250/13082
Fecha: 2009-03-27
Cita del item: MOLECULAR CELL, Volume: 33, Issue: 6, Pages: 679-691, 2009


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