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IRAK2 — NFKB1

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., Inflammation 1999 : Antisense IRAK-2 ODN inhibited IL-1 induced NF-KB activation and surface expression of ICAM-1 in a concentration ( 1-4 microg ) - and time ( 5-24 h ) -dependent fashion
Guo et al., Inflammation 2000 : IRAK-2 and PI 3-kinase synergistically activate NF-kappaB and AP-1 ... The effects of IRAK-2 or PI 3-kinase on NF-kappaB and AP-1 activation were confirmed by the results that overexpression of IRAK-2 failed to fully activate NF-kappaB and AP-1 and that overexpression of p110 PI 3-kinase is insufficient for NF-kappaB full activation but sufficient for AP-1 activation ... On the other hand, coexpression of IRAK-2 with p110 PI 3-kinase led to a synergistic activation of NF-kappaB and AP-1
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
Guo et al., Acta Pharmacol Sin 2000 : ( 2 ) Antisense IRAK-2 ODN inhibited IL-1 induced NF-kappa B activation in a concentration ( 1-8 micrograms ) - and time ( 5-24 h ) -dependent manner ... Antisense IRAK-2 ODN inhibited IL-1 induced NF-kappa B 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
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
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
Hardy et al., J Biol Chem 2004 : When overexpressed, Irak2a and Irak2b potentiated NF-kappaB activation by lipopolysaccharide
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
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
Bowie et al., Biochem Soc Trans 2008 : Further, I demonstrate how understanding one molecular mechanism whereby vaccinia virus inhibits NF-kappaB activation has led to a revealing of a key role for IRAK-2 in TRAF-6 mediated NF-kappaB activation
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
Wan et al., J Biol Chem 2009 (MAP Kinase Signaling System) : Although IRAK2 deficiency did not affect TLR4 mediated NFkappaB activation, a reduction of lipopolysaccharide (LPS) mediated mRNA stabilization contributed to the reduced cytokine and chemokine production observed in bone marrow derived macrophages from IRAK2-deficient mice
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 ... 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