Extrinsic and intrinsic apoptosis activate Pannexin-1 to drive NLRP3 inflammasome assembly

ABSTRACT: Pyroptosis is a form of lytic inflammatory cell death driven by inflammatory caspases-1, -4, -5 and -11. These caspases cleave and activate the pore-forming protein gasdermin D to induce membrane damage. By contrast, apoptosis is driven by apoptotic caspase-8 or -9 and has traditionally been classified as an immunologically silent form of cell death. Emerging evidence suggest that clinical inhibitors designed for cancer chemotherapy or inflammatory disorders such as SMAC mimetic, TAK1 inhibitors and BH3 mimetic promote caspase-8 or -9-dependent inflammatory cell death and NLRP3 inflammasome activation. However, the mechanism by which caspase-8 or -9 triggers cell lysis and NLRP3 activation is still undefined. Here, we demonstrate that during extrinsic apoptosis, caspase-8 cleaves GSDMD to

SUBMITTER: Prof. Petr Broz 

PROVIDER: S-SCDT-EMBOJ-2019-101638 | biostudies-other |

REPOSITORIES: biostudies-other