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IRF6 — RELB

Text-mined interactions from Literome

Mollah et al., J Immunol 2008 (Diabetes Mellitus, Type 1...) : In T1DM patients, late LPS mediated nuclear DNA binding by RelA, p50, c-Rel, and RelB was impaired as compared with type 2 DM, rheumatoid arthritis, and healthy subjects, associated with impaired DC CD40 and MHC class I induction but normal cytokine production
Saito et al., Biochem Biophys Res Commun 2010 (Lung Neoplasms...) : The activation of H69 cells by lipopolysaccharide (LPS) resulted in the induction of RelB and p100 expression
Bhattacharyya et al., Exp Cell Res 2010 : The pathway for LPS activation of RelB by the non-canonical pathway ( RelB ) in non-myeloid cells was not yet reported, but important for understanding the range of potential microbial LPS induced effects in inflammatory bowel disease
Benson et al., Toxicological sciences : an official journal of the Society of Toxicology 2011 : Both I3C and IO decreased basal levels of nuclear factor-kappa B p65, but only I3C suppressed the LPS induced activity of RelB
Deng et al., J Biol Chem 2013 : This is in sharp contrast to the well documented RelB stabilization and induction by high dose LPS , potentially through the phosphoinositide 3-kinase (PI3K) pathway ... Super low dose and high dose LPS cause opposing modulation of interleukin receptor associated kinase 1 and PI3K pathways and lead to opposing regulation of RelB