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NFKBIA — TLR4

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: NFKBIA → TLR4 (decreases) Hiratsuka et al., Nat Cell Biol 2008*
  Evidence: We found that SAA3–GST induced phosphorylation of I?B-? in macrophages derived from wild-type mice but not in those derived from TLR4 knockout (TLR4–/–) mice (Fig. 3f).

Text-mined interactions from Literome

Aki et al., Genes Cells 2005 : Furthermore, overall cellular tyrosine phosphorylation and TLR4 mediated activation of IkappaB-alpha , Erk and p38 but not of JNK, were also down-regulated in Csk knockdown cells
Mueller et al., J Immunol 2006 : TLR4/MD-2 mediated LPS uptake and TLR ligand induced I-kappaBalpha phosphorylation and IL-8 secretion were significantly diminished in Th2 cytokine primed IECs
Qin et al., J Biol Chem 2006 : On the other hand, TLR8 mediated IkappaBalpha phosphorylation, NF-kappaB, and JNK activation are completely abolished in MEKK3 ( -/- ) MEFs, whereas IL-1 mediated signaling was only moderately reduced in these deficient MEFs as compared with wild-type cells
Polumuri et al., J Immunol 2007 : Although TLR induced IkappaBalpha degradation was not affected by FcgammaR ligation, IkappaBalpha accumulated in the nuclei of cells treated with LPS and FcgammaR ligation for 4 h, and was blocked by PI3K inhibitors
Henning et al., J Immunol 2008 : SP-A decreases the phosphorylation of IkappaBalpha , a key regulator of NF-kappaB activity, and nuclear translocation of p65 which result in diminished TNF-alpha secretion in response to TLR ligands
Bhattacharyya et al., Inflamm Bowel Dis 2009 : DSS induced increases in phospho-IkappaBalpha , nuclear NFkappaB ( p65 ), and IL-8 secretion in human colonic epithelial cells in tissue culture are attributable to a reactive oxygen species ( ROS ) -induced pathway of inflammation, and do not require TLR4 , MyD88, or Bcl10, which are associated with the innate immune pathway of NFkappaB-IL-8 activation