Gene interactions and pathways from curated databases and text-mining

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IRAK1 — TLR2

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

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
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
Ahmad et al., Blood 2008 : Altogether, these results unequivocally show that HSV-1 induces TLR2 dependent activation of IL-15 gene expression, which requires the recruitment of both MyD88 and TIRAP/Mal and the activation of IRAK1 and TRAF6 leading to NF-kappaB translocation to the nucleus
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
Liu et al., J Immunol 2012 : Because IRAK1 is required for TLR7/9 induced IFN-I production, we propose that TLR2 signaling induces rapid depletion of IRAK1 , which impairs IFN-I induction by TLR7/9
Unger et al., PLoS Pathog 2012 (Haemophilus Infections...) : Rhinovirus attenuates non-typeable Hemophilus influenzae stimulated IL-8 responses via TLR2 dependent degradation of IRAK-1