Gene interactions and pathways from curated databases and text-mining

◀ Back to RELA

IRAK1 — RELA

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Vig et al., J Biol Chem 1999 : However, it is currently unknown whether mPLK/IRAK catalytic activity is required for IL-1 dependent NF-kappaB activation
Thomas et al., J Immunol 1999 (Hypersensitivity, Delayed...) : Activation of IRAK leads in turn to nuclear translocation of NF-kappaB , which directs expression of innate and adaptive immune response genes
Guo et al., Immunopharmacology 2000 : Antisense IRAK-1 oligonucleotide blocks activation of NF-kappa B and AP-1 induced by IL-18
Vig et al., J Biol Chem 2001 : These results lead us to propose a model in which SIMPL functions to regulate NF-kappaB activity by linking IRAK/mPLK to IKKbeta/alpha containing complexes
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
Maeda et al., J Biol Chem 2001 (Stomach Neoplasms) : In conclusion, H. pylori induced NF-kappaB activation in epithelial cells is dependent on cag PAI and contact but does not involve CD14 and IRAK , whereas in macrophage/monocytic cells it is independent of cag PAI or contact but involves CD14 and TLR4
Wald et al., Eur J Immunol 2001 : Furthermore, the death domain, but not the kinase activity of IRAK , is necessary for NFkappaB activation in response to IL-18
Bannerman et al., J Biol Chem 2002 : Together, these data suggest that the proximal signaling molecules involved in LPS induced NF-kappa B activation have a requisite involvement in LPS induced apoptosis and that the pathways leading to NF-kappa B activation and apoptosis diverge downstream of IRAK-1
Chen et al., J Biol Chem 2002 : CaMKKc and Akt overexpression decreases IRAK1 mediated NF-kappaB activity and its association with MyD88 in response to IL-1beta stimulation ... Furthermore, CaMKKc and Akt overexpression increases IRAK1 phosphorylation at Thr ( 100 ), and point mutation of this site abrogates the inhibitory effect of Akt on IRAK1 mediated NF-kappaB 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
Yeo et al., J Biol Chem 2003 : In contrast, overexpression of DN-IRAK1 or DN-TRAF6 only partially inhibited CpG DNA induced Cox-2 promoter activity and NF-kappaB activation, indicating the presence of additional signaling modulators downstream of MyD88
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
Bin et al., J Biol Chem 2003 : Moreover, TIRP mediated NF-kappaB activation is inhibited by dominant negative mutants of IRAK, IRAK-2 , TRAF6, and IKKbeta
Lee et al., J Biol Chem 2003 : Saturated fatty acid ( lauric acid ) -induced NFkappaB activation was inhibited by a dominant negative mutant of TLR4, MyD88, IRAK-1 , TRAF6, or IkappaBalpha in macrophages ( RAW264.7 ) and 293T cells transfected with TLR4 and MD2 ... Saturated fatty acid ( lauric acid ) -induced NFkappaB activation was inhibited by a dominant negative mutant of TLR4, MyD88, IRAK-1 , TRAF6, or IkappaBalpha in macrophages ( RAW264.7 ) and 293T cells transfected with TLR4 and MD2
Luftig et al., Proc Natl Acad Sci U S A 2003 : Epstein-Barr virus latent membrane protein 1 activation of NF-kappaB through IRAK1 and TRAF6 ... These data extend a role for IKKalpha in IKKbeta regulation, identify an unusual IKKbeta dependent and IKKgamma independent NF-kappaB activation, and indicate that IRAK1 and TRAF6 are essential for LMP1 induced NF-kappaB activation
Mamidipudi et al., J Biol Chem 2004 : We have previously shown that the activity of the interleukin-1 (IL-1) receptor associated kinase ( IRAK ) is required for nerve growth factor (NGF) induced activation of NF-kappaB and cell survival ( ( 2002 ) J. Biol. Chem. 277, 28010-28018 ) ... Moreover, transfection of kinase-dead iota PKC blocked both NGF- and IL-1 induced IRAK activation and the activity of NF-kappaB
Opitz et al., J Biol Chem 2004 : Additionally, dominant negative interleukin-1 receptor associated kinase 2, tumor necrosis factor receptor associated factor 6, NF-kappaB inducing kinase, transforming growth factor-beta activated kinase binding protein 2, and transforming growth factor-beta activated kinase 1 also inhibited Nod2 dependent NF-kappaB activation
Chen et al., Biochem Biophys Res Commun 2004 : Moreover, P6 induces MUC5AC transcription via TLR2-MyD88-IRAK1-TRAF6-TAK1 dependent p38 MAPK-AP1 and IKKbeta-IkappaBalpha-NF-kappaB signaling pathways
Rao et al., Mol Cell Biol 2005 (Inflammation) : Overexpression of IRAK1c suppressed NF-kappaB activation and blocked IL-1beta induced IL-6 as well as lipopolysaccharide- and CpG induced tumor necrosis factor alpha production in multiple cellular systems
Song et al., Proc Natl Acad Sci U S A 2006 : Because IRAK1 is upstream of TRAF6 in IL-1 activation of NF-kappaB, the potential role of IRAK1 in LMP1 mediated NF-kappaB activation through TRAF6 and inhibitor of kappaB (IkappaB) kinase ( IKK ) was initially investigated
Qin et al., J Biol Chem 2006 : The above results indicate that although TLR8 mediated NF-kappaB and JNK activation are IRAK dependent , they do not require IRAK modification and are TAK1 independent
Suzuki et al., Trends Immunol 2006 : Although each system seems to possess distinct activation mechanisms, interleukin-1 receptor associated kinase ( IRAK)-4 is essential for NF-kappaB activation in Toll-like receptor ( TLR ) and T-cell receptor ( TCR ) signaling pathways
Hartupee et al., J Biol Chem 2008 : IRAK1 , which is recognized to function upstream of TRAF6, is required for both mRNA stabilization and activation of NFkappaB
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
Dasu et al., Diabetes 2008 : High glucose increased TLR expression, myeloid differentiation factor 88, interleukin-1 receptor associated kinase-1 , and nuclear factor-kappaB (NF-kappaB) p65 dependent activation in THP-1 cells
Loiarro et al., J Biol Chem 2009 : GFP-MyD88- ( 27-72 ) exerted its effect by titrating IRAK1 and suppressing IRAK1 dependent NF-kappaB activation
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
Cui et al., J Biol Chem 2010 (Alzheimer Disease...) : Differential regulation of interleukin-1 receptor associated kinase-1 ( IRAK-1 ) and IRAK-2 by microRNA-146a and NF-kappaB in stressed human astroglial cells and in Alzheimer disease