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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