Show simple item record

Authordc.contributor.authorLisbona, Fernanda 
Authordc.contributor.authorRojas Rivera, Diego 
Authordc.contributor.authorThielen, Peter 
Authordc.contributor.authorZamorano, Sebastian 
Authordc.contributor.authorTodd, Derrick 
Authordc.contributor.authorMartinon, Fabio 
Authordc.contributor.authorGlavic Maurer, Álvaro 
Authordc.contributor.authorKress, Christina 
Authordc.contributor.authorLin, Jonathan H. 
Authordc.contributor.authorWalter, Peter 
Authordc.contributor.authorReed, John C. 
Authordc.contributor.authorGlimcher, Laurie H. 
Authordc.contributor.authorHetz Flores, Claudio 
Cita de ítemdc.identifier.citationMolecular Cell, Volumen 33, Issue 6, 2018, Pages 679-691
Abstractdc.description.abstractAdaptation 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 role for BI-1 in early adaptive responses against ER stress that contrasts with its known downstream function in apoptosis. ©
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
Link to Licensedc.rights.uri
Sourcedc.sourceMolecular Cell
Títulodc.titleBAX Inhibitor-1 Is a Negative Regulator of the ER Stress Sensor IRE1α
Document typedc.typeArtículo de revista
Indexationuchile.indexArtículo de publicación SCOPUS

Files in this item


This item appears in the following Collection(s)

Show simple item record

Attribution-NonCommercial-NoDerivs 3.0 Chile
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 Chile