Gene interactions and pathways from curated databases and text-mining

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IRF6 — PIK3CA

Text-mined interactions from Literome

Kristof et al., J Biol Chem 2003 (Inflammation) : The role of mTOR and PI3K in the activation of human inducible nitric oxide synthase transcription by cytokines and lipopolysaccharide (LPS) was investigated in lung epithelial adenocarcinoma ( A549 ) cells
Kim et al., J Immunol 2004 : TGF-beta1 was further found to decrease LPS induced activation of PI3K and Akt
Sheu et al., Cell Signal 2005 (Inflammation) : Both NO donor and LPS/IFN-gamma markedly activated the PI3K activity and the phosphorylation of Akt and nuclear factor (NF)-kappaB DNA binding activity in mesangial cells, which could be inhibited by LY294002 and transfection of dominant negative vectors of PI3K/p85 and Akt
Pan et al., Biochem Pharmacol 2006 (Cocarcinogenesis...) : We found that acacetin also inhibited LPS induced activation of PI3K/Akt and p44/42, but not p38 MAPK
Sherry et al., J Immunol 2007 (Diabetes Mellitus, Type 2) : LPS dependent stimulation of PI3K activity, ERK1/2 activation, and p38 kinase activity was greater in PerMphi from db/db mice as compared with db/+ mice
Liu et al., Biochim Biophys Acta 2007 (MAP Kinase Signaling System) : We propose that the inhibition of PI(3)K by wortmannin in mouse macrophages enhances the PI-PLC downstream signals, and subsequently increases the LPS induction of iNOS expression independently of Akt pathway
Donahue et al., Eur J Immunol 2007 : We used flow cytometry and magnetic cell sorting to examine the requirement for PI3K and mTOR in responses of splenic B cell subsets to BCR and LPS stimulation
Pan et al., J Agric Food Chem 2008 : We found that pterostilbene also inhibited LPS induced activation of PI3K/Akt , extracellular signal regulated kinase 1/2 and p38 MAPK
Pan et al., Mol Nutr Food Res 2008 : We found that 6-shogaol also inhibited LPS induced activation of PI3K/Akt and extracellular signal regulated kinase 1/2, but not p38 mitogen activated protein kinase ( MAPK )
Peairs et al., Clin Exp Immunol 2009 (Lupus Nephritis) : Mechanistically, AICAR inhibited the LPS/IFN-gamma stimulated PI3K/Akt signalling inflammatory cascade but did not affect LPS/IFN-gamma mediated inhibitory kappa B phosphorylation or nuclear factor (NF)-kappaB ( p65 ) nuclear translocation
Kuo et al., Mol Nutr Food Res 2009 : Inotilone also inhibited LPS induced activation of PI3K/Akt and extracellular signal regulated kinase 1/2 and p38 mitogen activated protein kinase
Lee et al., PloS one 2010 (Endotoxemia) : Furthermore, in vitro cellular studies demonstrated that LPS ( lipopolysaccharide ) activation of mTORC1-S6K still occurs in the presence of PI3K-Akt inhibition alone, but can be suppressed by concurrent inhibition of PI3K-Akt and MEK-ERK pathways
Hsu et al., Cancer Res 2011 (Colorectal Neoplasms...) : Taken together, the results indicate that stimulation of the TLR4/MD2 complex by LPS activates PI3K/AKT signaling and promotes downstream ß1 integrin function, thereby increasing the adhesiveness and metastatic capacity of CRC cells
Fortin et al., Eur J Immunol 2011 : Finally, we show that in LPS- and TNF activated neutrophils, PI3K acts downstream of the kinases p38 MAPK and TAK1
Maitra et al., J Immunol 2012 : Unlike high-dose LPS, low-dose LPS does not induce robust activation of NF-?B, MAPKs, PI3K , or anti-inflammatory mediators
Yang et al., J Mol Med (Berl) 2013 (Endotoxemia...) : LPS caused p38 MAPK-, JNK-, and PI3K/AKT mediated Mcl-1 stabilization and prevented apoptosis, and LPS induced GSK-3ß inactivation mainly through p38 MAPK and PI3K/AKT
Lee et al., J Cell Biochem 2013 : NaHS blocked nicotine and LPS induced activation of p38, ERK, MKP-1, PI3K , PKC, and PKC isoenzymes, and NF-?B
Hyam et al., Eur J Pharmacol 2013 : Arctigenin inhibited LPS induced PI3K , AKT and IKKß phosphorylation, but did not suppress LPS induced IRAK-1 phosphorylation
Chang et al., Microvasc Res 2013 : Homocysteine, but not LPS , blocked both PI3K activity and Slug expression in Notch activated cells, leading to increased endothelial apoptosis