| First Author | Vig E | Year | 1999 |
| Journal | J Biol Chem | Volume | 274 |
| Issue | 19 | Pages | 13077-84 |
| PubMed ID | 10224059 | Mgi Jnum | J:54893 |
| Mgi Id | MGI:1336566 | Doi | 10.1074/jbc.274.19.13077 |
| Citation | Vig E, et al. (1999) Modulation of tumor necrosis factor and interleukin-1-dependent NF-kappaB activity by mPLK/IRAK. J Biol Chem 274(19):13077-84 |
| abstractText | The innate immune response is an important defense against pathogenic agents. A component of this response is the NF-kappaB-dependent activation of genes encoding inflammatory cytokines such as interleukin-8 (IL-8) and cell adhesion molecules like E-selectin. Members of the serine/ threonine innate immune kinase family of proteins have been proposed to mediate the innate immune response. One serine/threonine innate immune kinase family member, the mouse Pelle-like kinase/ human interleukin-1 receptor-associated kinase (mPLK/IRAK), has been proposed to play an obligate role in promoting IL-1-mediated inflammation. However, it is currently unknown whether mPLK/ IRAK catalytic activity is required for IL-1-dependent NF-kappaB activation. The present study demonstrates that mPLK/IRAK catalytic activity is not required for IL-1-mediated activation of an NF-kappaB-dependent signal. Intriguingly, catalytically inactive mPLK/IRAK inhibits type 1 tumor necrosis factor (TNF) receptor-dependent NF-kappaB activation. The pathway through which mPLK/IRAK mediates this TNF response is TRADD- and TRAF2-independent. Our data suggest that in addition to its role in IL-1 signaling, mPLK/IRAK is a component of a novel signal transduction pathway through which TNF R1 activates NF-kappaB-dependent gene expression. |
