◀ Back to TLR4
IRAK2 — TLR4
Pathways - manually collected, often from reviews:
-
NCI Pathway Database Endogenous TLR signaling:
IRAK2 (IRAK2)
→
HMGB1/TLR4/MD2 (dimer)/MYD88/TIRAP complex (TLR4-LY96-HMGB1-MYD88-TIRAP)
(modification, collaborate)
Park et al., J Biol Chem 2004
Evidence: mutant phenotype, other species
-
NCI Pathway Database Endogenous TLR signaling:
IRAK2 (IRAK2)
→
HMGB1/TLR4/MD2 (dimer)/MYD88/TIRAP/IRAK/IRAK2/IRAK4 complex (TLR4-LY96-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/TLR4/MD2 (dimer)/MYD88/TIRAP complex (TLR4-LY96-HMGB1-MYD88-TIRAP)
→
HMGB1/TLR4/MD2 (dimer)/MYD88/TIRAP/IRAK/IRAK2/IRAK4 complex (TLR4-LY96-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/TLR4/MD2 (dimer)/MYD88/TIRAP/IRAK/IRAK2/IRAK4 complex (TLR4-LY96-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/TLR4/MD2 (dimer)/MYD88/TIRAP/IRAK/IRAK2/IRAK4 complex (TLR4-LY96-HMGB1-IRAK1-IRAK2-IRAK4-MYD88-TIRAP)
(modification, collaborate)
Park et al., J Biol Chem 2004
Evidence: mutant phenotype, other species
-
Reactome Reaction:
IRAK2
→
TLR4
(reaction)
Kollewe et al., J Biol Chem 2004, Rao et al., Mol Cell Biol 2005, Keating et al., J Biol Chem 2007, Gottipati et al., Cell Signal 2008, Kawagoe et al., Nat Immunol 2008, Wan et al., J Biol Chem 2009, Lin et al., Nature 2010, Flannery et al., J Biol Chem 2011
-
Reactome Reaction:
IRAK2
→
TLR4
(indirect_complex)
Rao et al., Mol Cell Biol 2005, Keating et al., J Biol Chem 2007, Gottipati et al., Cell Signal 2008, Kawagoe et al., Nat Immunol 2008, Wan et al., J Biol Chem 2009, Lin et al., Nature 2010, Flannery et al., J Biol Chem 2011
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
Keating et al., J Biol Chem 2007
:
Thus we propose that
IRAK-2 plays a more central role than IRAK-1 in
TLR signaling to NFkappaB
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
Uh et al., Reproductive biology and endocrinology : RB&E 2009
:
Here we investigated the
role of MyD88, TRIF and
IRAK2 on cAMP induced CRH promoter activation in JEG3 cells in the absence of
LPS/TLR4 stimulation
Flannery et al., J Biol Chem 2011
(MAP Kinase Signaling System) :
Thus IRAK-2 in mice and humans may function differently, and therefore we analyzed the
role of
IRAK-2 in
TLR responses in primary human cells ... siRNA knockdown of IRAK-2 expression in human peripheral blood mononuclear cells showed a
role for human
IRAK-2 in both
TLR4- and TLR8 mediated early NF?B and p38 MAPK activation and in induction of TNF mRNA ... Collectively, these data demonstrate for the first time an essential
role for
IRAK-2 in primary human cells for both transcriptional and post-transcriptional
TLR responses
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