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IRAK2 — TLR1
Pathways - manually collected, often from reviews:
-
NCI Pathway Database Endogenous TLR signaling:
IRAK2 (IRAK2)
→
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:
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/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
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
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
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 ... 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