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APP — IRF6

Text-mined interactions from Literome

Miklossy et al., Neurobiol Aging 2010 (Diabetes Mellitus, Type 2) : LPS increased APP in non-neuronal cells as well
Lee et al., Journal of neuroinflammation 2012 (Disease Models, Animal...) : Consistent with the inhibitory effect on neuroinflammation, 4-O-methylhonokiol inhibited LPS induced Aß1-42 generation, ß- and ?-secretase activities, and expression of amyloid precursor protein (APP) , BACE1 and C99 as well as activation of astrocytes and neuronal cell death in the brain, in cultured astrocytes and in microglial BV-2 cells
Lee et al., J Nutr Biochem 2013 (Alzheimer Disease...) : EGCG also suppressed LPS induced increase of the amyloid beta-peptide level and the expression of the amyloid precursor protein (APP) , ß-site APP cleaving enzyme 1 and its product C99
Mönning et al., FEBS Lett 1994 : LPS leads to an increase in cellular immature, non-amyloidogenic APP and secretion of also non-amyloidogenic APP fragments
Haziot et al., J Immunol 1998 : LPS ( endotoxin ) and proinflammatory cytokines ( IL-6, IL-1, and TNF-alpha ) are potent inducers of acute phase proteins (APP) ... Since LPS induces high levels of these cytokines after its interaction with CD14, a protein expressed on the surface of monocytes and neutrophils, it has been assumed that CD14 mediates the LPS induction of APP expression ... These studies show that the up-regulation of APP by LPS utilizes a non-CD14 receptor and requires a functional Lps gene