J Biol Chem 1999,
PMID: 10224059
Vig, E; Green, M; Liu, Y; Donner, D B; Mukaida, N; Goebl, M G; Harrington, M A
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.
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Text Mining Data
NF-kappaB → interleukin-1: "
Modulation of tumor necrosis factor and
interleukin-1 dependent
NF-kappaB activity by mPLK/IRAK
"
NF-kappaB → mPLK/IRAK: "
However, it is currently unknown whether mPLK/IRAK catalytic activity is required for IL-1 dependent NF-kappaB activation
"
NF-kappaB → IL-1: "
However, it is currently unknown whether mPLK/IRAK catalytic activity is required for IL-1 dependent NF-kappaB activation
"
NF-kappaB — tumor necrosis factor (TNF): "
Intriguingly, catalytically inactive mPLK/IRAK inhibits type 1 tumor necrosis factor (TNF) receptor dependent NF-kappaB activation
"
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