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IRAK1 — JUN
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Guo et al., Immunopharmacology 2000
:
Antisense
IRAK-1 oligonucleotide
blocks activation of NF-kappa B and
AP-1 induced by IL-18
Li et al., Proc Natl Acad Sci U S A 2001
:
Mutant I1A cells, lacking IL-1 receptor associated kinase (IRAK) mRNA and protein, have been used to study the
involvement of
IRAK in NFkappaB and
c-Jun N-terminal kinase (JNK) activation
Yanagisawa et al., Biochem J 2003
:
However,
IRAK-1-S overexpressed in 293T cells
induced constitutive activation of nuclear factor-kappaB (NF-kappaB) and
c-Jun N-terminal kinase (JNK) independent of stimulation by IL-1, as did IRAK-1-W
Dolganiuc et al., Gastroenterology 2004
(Hepatitis C...) :
HCV core and NS3 induced interleukin (IL)-1 receptor associated kinase (
IRAK ) activity, phosphorylation of p38, extracellular regulated ( ERK ), and c-jun N-terminal ( JNK ) kinases and induced
AP-1 activation
Chandrasekar et al., J Biol Chem 2005
:
Src kinase inhibitors PP1 and PP2, phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and LY294002, Akt inhibitor, the c-Jun N-terminal kinase (JNK) inhibitor SP600125, antisense JNK and dominant negative MyD88,
interleukin-1 receptor associated kinase ( IRAK)-1, IRAK4, and phosphatidylinositol 3-kinase expression all
attenuated IL-18 mediated
AP-1 binding and reporter activity, CXCL16 promoter-reporter activity, and CXCL16 expression
Song et al., Mol Immunol 2009
(Inflammation) :
In contrast, an inhibitor of both
IRAK-1 and IRAK-4 ( RO0884 ) reduced IL-1beta
induced p38 MAP kinase,
c-Jun N-terminal kinase activation, and IL-6 production in HUVEC
Merry et al., J Heart Lung Transplant 2010
(Lung Injury...) :
Lungs were assessed for vascular permeability, myeloperoxidase content, bronchoalveolar lavage inflammatory cell and cytokine/chemokine content, as well as nuclear translocation of nuclear factor kappaB (NFkappaB) and
activator protein-1 (AP-1) , and
interleukin-1 receptor associated kinase-1 ( IRAK-1 ) and stress activated protein kinase ( SAPK )
activation
Chiou et al., Biochem Pharmacol 2011
:
In conclusion, TH-4-PX
inhibited LPS induced NF-?B and
AP-1 activations by interfering with the posttranslational modification ( phosphorylation and/or ubiquitinylation ) of
IRAK-1 in the cell membrane to impede TAK1 mediated activation of IKK and MAPKs signal transduction
Yang et al., J Ethnopharmacol 2013
:
In addition, the observed downregulation of
activator protein (AP)-1 and cAMP response element binding ( CREB ) was
due to the direct inhibition of
interleukin-1 receptor associated kinase ( IRAK)1 and IRAK4, which was also linked to the suppression of c-Jun N-terminal kinase (JNK) and p38