Gene interactions and pathways from curated databases and text-mining

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IRAK3 — IRF6

Text-mined interactions from Literome

Yamashina et al., Biochem Biophys Res Commun 2000 : In Kupffer cells from mice treated with ethanol 1 h earlier, LPS induced TNFalpha production, and IRAK expression and activity and NFkappaB were decreased 50-60 % of control
Ferlito et al., J Leukoc Biol 2001 (Leukemia, Monocytic, Acute...) : LPS stimulation induced production of TNF-alpha or TxB2 and degradation of IRAK
Bannerman et al., J Biol Chem 2002 : Using a variety of dominant negative constructs, we have identified a role for MyD88 and interleukin-1 receptor associated kinase-1 ( IRAK-1 ) in mediating LPS pro-apoptotic signaling in human endothelial cells
Taggart et al., J Biol Chem 2002 : We have also demonstrated that SLPI prevents LPS induced interleukin-1 receptor associated kinase and IkappaBbeta degradation
Ferlito et al., J Endotoxin Res 2002 : Neither PTx nor PP2 inhibited LPS induced activation of interleukin receptor activated kinase ( IRAK ) or inhibited translocation of NF-kappaB
Yamashina et al., Nihon Arukoru Yakubutsu Igakkai Zasshi 2003 (Liver Diseases, Alcoholic) : In contrast, in Kupffer cells from mice treated with ethanol 21 hours earlier, LPS induced TNF alpha production, expression and activity of IRAK were increased 1.5-fold over controls, while NF kappa B activation was elevated 3-fold
Noubir et al., J Biol Chem 2004 : Lipopolysaccharide (LPS) signaling leading to nuclear factor-kappaB activation in mononuclear phagocytes involves interleukin-1 receptor associated kinase ( IRAK ), which is rapidly activated after exposure to agonist
Cuschieri et al., Cell Immunol 2004 : LPS stimulation led to the phosphorylation and degradation of IRAK , followed by activation of JNK/SAPK, ERK 1/2, and p38 ... Proteasome inhibition with either lactacystin or MG-132 attenuated LPS induced IRAK degradation, and enhanced activation of JNK/SAPK, ERK 1/2, and p38
Frost et al., Am J Physiol Cell Physiol 2004 (MAP Kinase Signaling System) : LPS transiently stimulated the phosphorylation of the interleukin-1 receptor associated kinase ( IRAK-1 ) in C ( 2 ) C ( 12 ) cells and decreased the total amount of IRAK-1 both in vitro and in vivo over time
Cuschieri et al., J Surg Res 2004 : LPS stimulation led to the mobilization of TLR4 to lipid rafts followed by phosphorylation and activation of IRAK , ERK 1/2, p38, and JNK/SAPK
Li et al., J Leukoc Biol 2006 : Furthermore, decreased MyD88-IRAK immunocomplex formation, as demonstrated by immunoprecipitation, was observed in BLP-tolerant cells following a second BLP or LPS stimulation
van 't Veer et al., J Immunol 2007 (Endotoxemia) : In vitro studies in whole blood showed that IRAK-M up-regulation by LPS is largely dependent on TNF-alpha
Domon et al., J Leukoc Biol 2008 : Early and preferential induction of IL-1 receptor associated kinase-M in THP-1 cells by LPS derived from Porphyromonas gingivalis ... Degradation of IRAK-1 was more obvious in E. coli LPS stimulated macrophages than the cells stimulated with P. gingivalis LPS, suggesting that P. gingivalis LPS induced IRAK-M suppressed dissociation of IRAK-1 from the receptor complex, resulting in escape from subsequent degradation
Kim et al., J Immunol 2008 (MAP Kinase Signaling System...) : In this study, the effect of Lactobacillus plantarum lipoteichoic acid ( pLTA ) on LPS induced MAPK activation, NF-kappaB activation, and the expression of TNF-alpha and IL-1R associated kinase M (IRAK-M) was examined ... These changes were accompanied by the suppression of the LPS induced expression of TLR4, NOD1, and NOD2, and the induction of IRAK-M , with a concurrent reduction of TNF-alpha secretion
Sebai et al., Arch Biochem Biophys 2010 : LPS increased CD14 expression ; IRAK1 and a phosphorylated form of p38 MAPK protein
Reis et al., Cell Biochem Biophys 2011 : TNF-a is induced by LPS in the LMP knockout macrophages because I?B and IRAK are degraded normally via the MyD88 pathway
Nguyen et al., Am J Physiol Lung Cell Mol Physiol 2012 (Inflammation) : Surfactant mediated upregulation of IRAK-M in macrophages suppresses TLR4 mediated TNF-a and IL-6 production in response to LPS , and IRAK-M knockdown by small interfering RNA reverses this suppression