| First Author | Subramanian N | Year | 2013 |
| Journal | Cell | Volume | 153 |
| Issue | 2 | Pages | 348-61 |
| PubMed ID | 23582325 | Mgi Jnum | J:197368 |
| Mgi Id | MGI:5492224 | Doi | 10.1016/j.cell.2013.02.054 |
| Citation | Subramanian N, et al. (2013) The adaptor MAVS promotes NLRP3 mitochondrial localization and inflammasome activation. Cell 153(2):348-61 |
| abstractText | NLRP3 is a key component of the macromolecular signaling complex called the inflammasome that promotes caspase 1-dependent production of IL-1beta. The adaptor ASC is necessary for NLRP3-dependent inflammasome function, but it is not known whether ASC is a sufficient partner and whether inflammasome formation occurs in the cytosol or in association with mitochondria is controversial. Here, we show that the mitochondria-associated adaptor molecule, MAVS, is required for optimal NLRP3 inflammasome activity. MAVS mediates recruitment of NLRP3 to mitochondria, promoting production of IL-1beta and the pathophysiologic activity of the NLRP3 inflammasome in vivo. Our data support a more complex model of NLRP3 inflammasome activation than previously appreciated, with at least two adapters required for maximal function. Because MAVS is a mitochondria-associated molecule previously considered to be uniquely involved in type 1 interferon production, these findings also reveal unexpected polygamous involvement of PYD/CARD-domain-containing adapters in innate immune signaling events. |
