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IRAK4 — TLR2

Pathways - manually collected, often from reviews:

• NCI Pathway Database Endogenous TLR signaling: IRAK2 (IRAK2) → HMGB1/TLR2/TLR1/MYD88/TIRAP/IRAK/IRAK2/IRAK4 complex (TLR2-TLR1-HMGB1-IRAK1-IRAK2-IRAK4-MYD88-TIRAP) (modification, collaborate)
  Park et al., J Biol Chem 2004
  Evidence: mutant phenotype, other species
• NCI Pathway Database Endogenous TLR signaling: IRAK4 (IRAK4) → HMGB1/TLR2/TLR1/MYD88/TIRAP complex (TLR2-TLR1-HMGB1-MYD88-TIRAP) (modification, collaborate)
  Park et al., J Biol Chem 2004
  Evidence: mutant phenotype, other species
• NCI Pathway Database Endogenous TLR signaling: IRAK4 (IRAK4) → HMGB1/TLR2/TLR1/MYD88/TIRAP/IRAK/IRAK2/IRAK4 complex (TLR2-TLR1-HMGB1-IRAK1-IRAK2-IRAK4-MYD88-TIRAP) (modification, collaborate)
  Park et al., J Biol Chem 2004
  Evidence: mutant phenotype, other species
• NCI Pathway Database Endogenous TLR signaling: IRAK (IRAK1) → HMGB1/TLR2/TLR1/MYD88/TIRAP/IRAK/IRAK2/IRAK4 complex (TLR2-TLR1-HMGB1-IRAK1-IRAK2-IRAK4-MYD88-TIRAP) (modification, collaborate)
  Park et al., J Biol Chem 2004
  Evidence: mutant phenotype, other species
• NCI Pathway Database Endogenous TLR signaling: HMGB1/TLR2/TLR1/MYD88/TIRAP complex (TLR2-TLR1-HMGB1-MYD88-TIRAP) → HMGB1/TLR2/TLR1/MYD88/TIRAP/IRAK/IRAK2/IRAK4 complex (TLR2-TLR1-HMGB1-IRAK1-IRAK2-IRAK4-MYD88-TIRAP) (modification, collaborate)
  Park et al., J Biol Chem 2004
  Evidence: mutant phenotype, other species
• Reactome Reaction: TLR2 → IRAK4 (indirect_complex) Li et al., Proc Natl Acad Sci U S A 2002, Suzuki et al., Trends Immunol 2002, Cheng et al., Biochem Biophys Res Commun 2007, Kawagoe et al., J Exp Med 2007, Moncrieffe et al., J Biol Chem 2008*, Towb et al., J Innate Immun 2009*, Motshwene et al., J Biol Chem 2009, Lin et al., Nature 2010
• Reactome Reaction: TLR2 → IRAK4 (reaction) Li et al., Proc Natl Acad Sci U S A 2002, Suzuki et al., Trends Immunol 2002, Kollewe et al., J Biol Chem 2004, Cheng et al., Biochem Biophys Res Commun 2007, Kawagoe et al., J Exp Med 2007, Kawagoe et al., Nat Immunol 2008, Moncrieffe et al., J Biol Chem 2008*, Towb et al., J Innate Immun 2009*, Motshwene et al., J Biol Chem 2009, Lin et al., Nature 2010

Text-mined interactions from Literome

Bulut et al., J Immunol 2001 : Cooperation of Toll-like receptor 2 and 6 for cellular activation by soluble tuberculosis factor and Borrelia burgdorferi outer surface protein A lipoprotein : role of Toll interacting protein and IL-1 receptor signaling molecules in Toll-like receptor 2 signaling
Jacinto et al., J Immunol 2002 : Correspondingly, stimulation of TLR2 by LTA, although activating IRAK, does not cause IRAK degradation
Kobayashi et al., Cell 2002 (Salmonella Infections) : Thus, IRAK-M regulates TLR signaling and innate immune homeostasis
Hazeki et al., Eur J Immunol 2003 : PP2, an inhibitor of Src family tyrosine kinases, prevented the TLR induced phosphorylation of paxillin and Pyk2 without affecting TLR induced IRAK activation
Hatao et al., J Leukoc Biol 2004 : We found that stimulation of TLR2, TLR4 , or TLR9, but not TLR3, caused a decrease in IRAK-4 protein without affecting its mRNA level in a mouse macrophage cell line, RAW 264 ... We found that stimulation of TLR2 , TLR4, or TLR9, but not TLR3, caused a decrease in IRAK-4 protein without affecting its mRNA level in a mouse macrophage cell line, RAW 264
Zhang et al., Infect Immun 2005 (Pseudomonas Infections) : We also determined that MyD88, IRAK , TRAF6, and Toll interacting protein (Tollip), but not TIRAP, were involved in the TLR mediated response to P. aeruginosa in HAECs
Pathak et al., Nat Immunol 2007 : Direct binding of ESAT-6 to TLR2 activated Akt and prevented interaction between the adaptor MyD88 and ` downstream ' kinase IRAK4 , thus abrogating NF-kappaB activation
Hatao et al., FEMS Immunol Med Microbiol 2008 : IRAK-4 plays an essential role in Toll-like receptor ( TLR ) /IL-1 receptor signaling
Staschke et al., J Immunol 2009 (Encephalomyelitis, Autoimmune, Experimental) : The IL-1R associated kinase 4 (IRAK4) is critical for IL-1/TLR signaling
Pennini et al., J Immunol 2013 (Genetic Predisposition to Disease...) : IRAK4 is critical for MyD88 dependent TLR signaling, and patients with Irak4 mutations are extremely susceptible to recurrent bacterial infections ... Importantly, we identified two kinases downstream of the MAPKs, MNK1 and MSK1, whose phosphorylation is deficient in IRAK4 ( KDKI ) macrophages stimulated through either TLR2 or TLR4, suggesting that IRAK4 contributes to TLR signaling beyond the initial phosphorylation of MAPKs
von Bernuth et al., Eur J Immunol 2012 (Bacterial Infections...) : By contrast, human TLR- and IL-1R dependent immunity mediated by MyD88 and IRAK-4 seems to be effective in the natural setting against only a few bacteria and is most important in infancy and early childhood