BAX and BAK at the Gates of Innate Immunity

Lorenzo Galluzzi; Claire Vanpouille-Box

doi:10.1016/j.tcb.2018.02.010

BAX and BAK at the Gates of Innate Immunity

Trends Cell Biol. 2018 May;28(5):343-345. doi: 10.1016/j.tcb.2018.02.010. Epub 2018 Mar 16.

Authors

Lorenzo Galluzzi¹, Claire Vanpouille-Box²

Affiliations

¹ Department of Radiation Oncology, Weill Cornell Medical College, New York, NY, USA; Sandra and Edward Meyer Cancer Center, New York, NY, USA; Université Paris Descartes/Paris V, Paris, France. Electronic address: deadoc@vodafone.it.
² Department of Radiation Oncology, Weill Cornell Medical College, New York, NY, USA. Electronic address: clv2002@med.cornell.edu.

PMID: 29555208
DOI: 10.1016/j.tcb.2018.02.010

Abstract

Large BAX/BAK pores that form during apoptosis enable mitochondrial nucleoids to access the cytosol, potentially leading to inflammatory signaling via CGAS. Under physiological conditions, however, BAX/BAK-dependent caspase activation rapidly dismantles dying cells to prevent inflammatory responses. BAX and BAK operate at the interface between apoptotic signaling and innate immunity control.

Keywords: STING; cytochrome c; mitochondrial outer membrane permeabilization; mtDNA; regulated cell death; type I interferon.

Publication types

Research Support, Non-U.S. Gov't
Comment

MeSH terms

Apoptosis
DNA, Mitochondrial*
Immunity, Innate
Mitochondria
bcl-2 Homologous Antagonist-Killer Protein
bcl-2-Associated X Protein*

Substances

DNA, Mitochondrial
bcl-2 Homologous Antagonist-Killer Protein
bcl-2-Associated X Protein