Gene interactions and pathways from curated databases and text-mining

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IRAK1 — 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
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
Kubo-Murai et al., J Biochem 2008 : Stimulation of these cells with TLR ligands did not cause the degradation of IRAK-1 , which was clearly observed in the parent cells
Kawagoe et al., Nat Immunol 2008 : Thus, IRAK2 is critical in late-phase TLR responses , and IRAK1 and IRAK2 are essential for the initial responses to TLR stimulation
Nguyen et al., Cell Signal 2009 : Phosphorylation of IRAK-1 by IRAK-4 in response to TLR activation may then release IRAK-1 from the inhibitory constraint exerted by its C-terminal domain
Cho et al., J Cell Physiol 2010 (Calcinosis) : Overexpression of miR-146a induced the inhibition of IRAK1 expression and inhibited basal and TNF-alpha- and TLR ligand induced osteogenic differentiation
Kar et al., Eur J Immunol 2011 (Inflammation...) : Analysis of upstream signaling events revealed that TLR 2/4 mediated MyD88 dependent participation of IL-1R activated kinase (IRAK)1 , TNF receptor associated factor (TRAF)6 and TGFß activated kinase (TAK)1 is essential to induce cystatin mediated I?B kinase ( IKK ) /NF-?B activation in macrophages
Kumar Pachathundikandi et al., PloS one 2011 (Helicobacter Infections) : Using phospho-specific antibodies and luciferase reporter assays, we further demonstrate that H. pylori induces IRAK-1 and I?B phosphorylation in a TLR dependent manner, and this was required for activation of transcription factor NF-?B
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 ... We show that while IRAK2 is redundant for TLR4 signaling, IRAK1 is essential for TLR4 signaling in mast cells