Gene interactions and pathways from curated databases and text-mining

◀ Back to IRF6

IRF6 — MYLIP

Text-mined interactions from Literome

Tili et al., J Immunol 2007 (Shock, Septic) : LPS stimulation of mouse Raw 264.7 macrophages resulted in the up-regulation of miR-155 and down-regulation of miR-125b levels ... Altogether, our data suggest that the LPS/TNF-alpha dependent regulation of miR-155 and miR-125b may be implicated in the response to endotoxin shock, thus offering new targets for drug design
Bazzoni et al., Proc Natl Acad Sci U S A 2009 (Inflammation) : Among the 3 different genes encoding miR-9 precursors in humans, we show that LPS selectively induces the transcription of miR-9-1 located in the CROC4 locus, in a MyD88- and NF-kappaB dependent manner
Schmelzer et al., Mediators Inflamm 2009 : Preincubation of human monocytic THP-1 cells with ubiquinol-10 reduced the LPS induced expression level of miR-146a to 78.9 +/- 13.22 % ... In liver samples of mice injected with LPS, supplementation with ubiquinol-10 leads to a reduction of LPS induced miR-146a expression to 78.12 +/- 21.25 %
Jennewein et al., J Biol Chem 2010 : We provide evidence that LPS induced miR-27b contributes to destabilization of PPARgamma1 mRNA
Murphy et al., J Immunol 2010 : LPS induces let-7a and inhibits miR-125b expression in human macrophages, and pretreatment with estradiol abrogates these effects
Tili et al., Carcinogenesis 2010 : Finally, we show that resveratrol impairs the upregulation of miR-155 by LPS in a miR-663 dependent manner
Roderburg et al., Hepatology 2011 (Carbon Tetrachloride Poisoning...) : On a cellular level, down-regulation of miR-29 in murine hepatic stellate cells ( HSCs ) was mediated by transforming growth factor beta ( TGF-ß ) as well as inflammatory signals, namely, lipopolysaccharide (LPS) and nuclear factor kappa B ( NF-?B )
Thompson et al., J Biol Chem 2011 (Lymphoma, Large B-Cell, Diffuse) : Additionally, miR-155 is induced by LPS treatment or expression of the CARD11 mutant in BJAB cells
Jiang et al., Cell Biochem Funct 2011 : These results suggested that the expression of miR-17-3p and miR-106a is regulated by TNFa and LPS in HeLa cells
Hennessy et al., J Biol Chem 2011 : We have therefore identified a mechanism for LPS signaling which involves a decrease in miR-107 leading to an increase in CDK6
Zhou et al., PloS one 2012 (MAP Kinase Signaling System) : LPS stimulation activated miR-16 gene transcription in human monocytes ( U937 ) and biliary epithelial cells ( H69 ) through MAPK dependent mechanisms
Zeng et al., Zhongguo Wei Zhong Bing Ji Jiu Yi Xue 2012 : To study the effects of Shenfu injection ( SF ) on the expression of lipopolysaccharide(LPS) induced microRNA-146a (miR-146a) in rat alveolar macrophages ( AMs ), and to extrapolate its potential anti-inflammatory mechanisms
Nahid et al., J Immunol 2013 : During bacterial infection, PGN mediated TLR2 signaling induces miR-132/-212 to downregulate IRAK4, an early component in the MyD88 dependent pathway, whereas LPS/TLR4 induced miR-146a downregulates downstream components of the same MyD88 dependent pathway
Xue et al., Placenta 2013 : Here we demonstrated that miR-155* , induced by lipopolysaccharide (LPS) in an AP-1/NF-?B dependent manner, played a positive feedback role in AP-1/NF-?B pathway via targeting interleukin-1 receptor associated kinase M ( IRAKM ) and NF-?B inhibitor interacting Ras-like 1 ( NKIRAS1 ) in trophoblasts
Lee et al., Oncogenesis 2013 : In conclusion, our study for the first time reveals the contribution of miR-26a-2 to LPS tumorigenesis, partly through inhibiting RCBTB1, suggesting that miR-26a-2 is a novel therapeutic target for human LPS
Zhou et al., PloS one 2013 : Induction of CX3CL1 and downregulation of miR-424 and miR-503 were also detected in epithelial cells in response to LPS stimulation
Olivieri et al., Free Radic Biol Med 2013 (Inflammation) : However, short-term CoQ10H2 supplementation attenuated LPS induced MIRAKIL changes in young cells ; in senescent cells CoQ10H2 supplementation significantly attenuated LPS induced miR-146a and IRAK-1 modulation but failed to curb IL-6 release