◀ Back to IRF6
IRAK2 — IRF6
Text-mined interactions from Literome
Yamashina et al., Biochem Biophys Res Commun 2000
:
In Kupffer cells from mice treated with ethanol 1 h earlier,
LPS induced TNFalpha production, and
IRAK expression and activity and NFkappaB were decreased 50-60 % of control
Ferlito et al., J Leukoc Biol 2001
(Leukemia, Monocytic, Acute...) :
LPS stimulation
induced production of TNF-alpha or TxB2 and degradation of
IRAK
Bannerman et al., J Biol Chem 2002
:
Using a variety of dominant negative constructs, we have identified a
role for MyD88 and
interleukin-1 receptor associated kinase-1 ( IRAK-1 ) in mediating
LPS pro-apoptotic signaling in human endothelial cells
Taggart et al., J Biol Chem 2002
:
We have also demonstrated that SLPI prevents
LPS induced
interleukin-1 receptor associated kinase and IkappaBbeta degradation
Ferlito et al., J Endotoxin Res 2002
:
Neither PTx nor PP2 inhibited
LPS induced
activation of interleukin receptor activated kinase (
IRAK ) or inhibited translocation of NF-kappaB
Yamashina et al., Nihon Arukoru Yakubutsu Igakkai Zasshi 2003
(Liver Diseases, Alcoholic) :
In contrast, in Kupffer cells from mice treated with ethanol 21 hours earlier,
LPS induced TNF alpha production, expression and activity of
IRAK were increased 1.5-fold over controls, while NF kappa B activation was elevated 3-fold
Noubir et al., J Biol Chem 2004
:
Lipopolysaccharide (LPS) signaling leading to nuclear factor-kappaB activation in mononuclear phagocytes
involves interleukin-1 receptor associated kinase ( IRAK ), which is rapidly activated after exposure to agonist
Cuschieri et al., Cell Immunol 2004
:
LPS stimulation
led to the phosphorylation and degradation of
IRAK , followed by activation of JNK/SAPK, ERK 1/2, and p38 ... Proteasome inhibition with either lactacystin or MG-132 attenuated
LPS induced
IRAK degradation, and enhanced activation of JNK/SAPK, ERK 1/2, and p38
Frost et al., Am J Physiol Cell Physiol 2004
(MAP Kinase Signaling System) :
LPS transiently
stimulated the phosphorylation of the
interleukin-1 receptor associated kinase ( IRAK-1 ) in C ( 2 ) C ( 12 ) cells and decreased the total amount of IRAK-1 both in vitro and in vivo over time
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
Li et al., J Leukoc Biol 2006
:
Furthermore, decreased
MyD88-IRAK immunocomplex formation, as demonstrated by immunoprecipitation, was
observed in BLP-tolerant cells following a second BLP or
LPS stimulation
Wan et al., J Biol Chem 2009
(MAP Kinase Signaling System) :
Moreover,
LPS stimulation
induced an interaction of
IRAK2 with TRAF6, MKK3/6, and MK2, implicating a critical role for mitogen activated protein kinase signaling in LPS induced IRAK2 mediated post-transcriptional control
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
Sebai et al., Arch Biochem Biophys 2010
:
LPS increased CD14 expression
; IRAK1 and a phosphorylated form of p38 MAPK protein
Reis et al., Cell Biochem Biophys 2011
:
TNF-a is
induced by
LPS in the LMP knockout macrophages because I?B and
IRAK are degraded normally via the MyD88 pathway