BAX inhibitor-1 regulates autophagy by controlling the IRE1α branch of the unfolded protein response

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dc.contributor.authorCastillo, Karen
dc.contributor.authorRojas-Rivera, Diego
dc.contributor.authorLisbona, Fernanda
dc.contributor.authorCaballero, Benjamin
dc.contributor.authorNassif, Melissa
dc.contributor.authorCourt, Felipe A.
dc.contributor.authorSchuck, Sebastian
dc.contributor.authorIbar, Consuelo
dc.contributor.authorWalter, Peter
dc.contributor.authorSierralta, Jimena
dc.contributor.authorGlavic, Alvaro
dc.contributor.authorHetz, Claudio
dc.date.accessioned2025-01-21T00:00:14Z
dc.date.available2025-01-21T00:00:14Z
dc.date.issued2011
dc.description.abstractBoth autophagy and apoptosis are tightly regulated processes playing a central role in tissue homeostasis. Bax inhibitor 1 (BI-1) is a highly conserved protein with a dual role in apoptosis and endoplasmic reticulum (ER) stress signalling through the regulation of the ER stress sensor inositol requiring kinase 1 alpha (IRE1 alpha). Here, we describe a novel function of BI-1 in the modulation of autophagy. BI-1-deficient cells presented a faster and stronger induction of autophagy, increasing LC3 flux and autophagosome formation. These effects were associated with enhanced cell survival under nutrient deprivation. Repression of autophagy by BI-1 was dependent on cJun-N terminal kinase (JNK) and IRE1 alpha expression, possibly due to a displacement of TNF-receptor associated factor-2 (TRAF2) from IRE1 alpha. Targeting BI-1 expression in flies altered autophagy fluxes and salivary gland degradation. BI-1 deficiency increased flies survival under fasting conditions. Increased expression of autophagy indicators was observed in the liver and kidney of bi-1-deficient mice. In summary, we identify a novel function of BI-1 in multicellular organisms, and suggest a critical role of BI-1 as a stress integrator that modulates autophagy levels and other interconnected homeostatic processes. The EMBO Journal (2011) 30, 4465-4478. doi:10.1038/emboj.2011.318; Published online 16 September 2011
dc.fuente.origenWOS
dc.identifier.doi10.1038/emboj.2011.318
dc.identifier.eissn1460-2075
dc.identifier.issn0261-4189
dc.identifier.urihttps://doi.org/10.1038/emboj.2011.318
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/95331
dc.identifier.wosidWOS:000296716600013
dc.issue.numero21
dc.language.isoen
dc.pagina.final4478
dc.pagina.inicio4465
dc.revistaEmbo journal
dc.rightsacceso restringido
dc.subjectautophagy
dc.subjectbax inhibitor-1(B1-1)
dc.subjectinositol requiring kinase 1 alpha (IRE1 alpha)
dc.subjectjun-terminal kinase (JNK)
dc.subjectmicrotubule-associated protein 1 light chain 3 (LC3)
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleBAX inhibitor-1 regulates autophagy by controlling the IRE1α branch of the unfolded protein response
dc.typeartículo
dc.volumen30
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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