Gene interactions and pathways from curated databases and text-mining

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IRAK4 — TLR4

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

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
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
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
Hatao et al., FEMS Immunol Med Microbiol 2008 : IRAK-4 plays an essential role in Toll-like receptor ( TLR ) /IL-1 receptor signaling
Koziczak-Holbro et al., Ernst Schering Foundation symposium proceedings 2007 : In summary, our results suggest that IRAK-4 kinase activity plays a critical role in IL-1R-, TLR4- , and TLR7 mediated induction of inflammatory responses
Singh et al., J Immunol 2009 (Common Variable Immunodeficiency) : We observed impaired O ( 2 ) ( ) generation by LPS treated and fMLP activated IRAK4-deficient PMN that correlated with decreased phosphorylation of p47(phox) and subnormal translocation of p47(phox), p67(phox), Rac2, and gp91(phox)/Nox2 to the membranes indicating that TLR4 signaling to the NOX activation pathway requires IRAK4
Staschke et al., J Immunol 2009 (Encephalomyelitis, Autoimmune, Experimental) : The IL-1R associated kinase 4 (IRAK4) is critical for IL-1/TLR signaling
Gao et al., Crit Care Med 2012 (Sepsis) : CLP-activation of TLR4 mediated nuclear factor-?B and Toll/IL-1 receptor-domain containing adapter inducing interferon-ß-dependant interferon signaling pathways was prevented by TLR3 deficiency
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
Sandig et al., Eur J Immunol 2013 : We show that while IRAK2 is redundant for TLR4 signaling, IRAK1 is essential for TLR4 signaling in mast cells