| First Author | Chen KW | Year | 2020 |
| Journal | Eur J Immunol | Volume | 50 |
| Issue | 2 | Pages | 170-177 |
| PubMed ID | 31411729 | Mgi Jnum | J:287943 |
| Mgi Id | MGI:6390696 | Doi | 10.1002/eji.201948254 |
| Citation | Chen KW, et al. (2020) Pannexin-1 promotes NLRP3 activation during apoptosis but is dispensable for canonical or noncanonical inflammasome activation. Eur J Immunol 50(2):170-177 |
| abstractText | Inflammasomes are multimeric protein complex that assemble in the cytosol upon microbial infection or cellular stress. Upon activation, inflammasomes drive the maturation of proinflammatory cytokines, IL-1beta and IL-18, and also activate the pore-forming protein, gasdermin D to initiate a form of lytic cell death known as "pyroptosis". Pannexin-1 is channel-forming glycoprotein that promotes membrane permeability and ATP release during apoptosis; and was implicated in canonical NLRP3 or noncanonical inflammasome activation. Here, by utilizing three different pannexin-1 channel inhibitors and two lines of Panx1(-/-) macrophages, we provide genetic and pharmacological evidence that pannexin-1 is dispensable for canonical or noncanonical inflammasome activation. In contrast, we demonstrate that pannexin-1 cleavage and resulting channel activity during apoptosis promotes NLRP3 inflammasome activation. |
