Gene interactions and pathways from curated databases and text-mining

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IRF6 — POLDIP2

Text-mined interactions from Literome

Yang et al., J Biol Chem 2000 : When MD-2, a protein associated with the extracellular domain of TLR4, was expressed in these cells, there was a marked increase in Elk-1 activity as well as ERK, JNK, and p38 MAP kinase phosphorylation in response to LPS
Kim et al., Brain Res 2000 (Glioma) : Furthermore, LPS plus CHX enhanced phosphorylation of ERK, p38 , and CREB in a synergistic manner
Ferlito et al., Shock 2001 (MAP Kinase Signaling System) : LPS desensitized cells exhibited augmented IkappaB alpha content and were refractory to LPS induced IkappaB alpha degradation and p38 phosphorylation
Won et al., Brain Res Mol Brain Res 2001 (Glioma) : Furthermore, LPS induced increases of p-p38 , but not activation of NF kappa B, were also reduced by FSK and H89 reversed the FSK induced inhibition response
Hsu et al., J Immunol 2001 : In addition, LPS induced PKC and p38 mitogen activated protein kinase activation were overcome by ceramide
Kim et al., Nitric Oxide 2002 : In contrast, mercury activated p38 mitogen activated protein kinase ( p38 MAPK ) and additively increased LPS induced p38 MAPK phosphorylation
Medvedev et al., J Immunol 2002 : Pretreatment of human monocytes with LPS decreased LPS mediated NF-kappaB activation, p38 mitogen activated protein kinase phosphorylation, and TNF-alpha gene expression, documenting the induction of endotoxin tolerance
Nakamura et al., Inflamm Res 2003 : LPS activated Erk-1/2 and p38 levels, by 4.7-fold and 1.8-fold, respectively ( P < 0.05 ), which were suppressed by terbutaline ( 10 ( -6 ) - 10 ( -8 ) M ) in a dose dependent way
Takada et al., J Biol Chem 2003 : LPS activated C-Jun N-terminal kinase, p38MAPK , and extracellular signal regulated kinase in wt cells, but the levels were much higher in p60-/-, p80-/-, and p60-/- p80-/- cells
Xia et al., Scand J Immunol 2003 : We also found that LPS or LPS plus IFN-gamma significantly enhanced the phosphorylation of extracellular signal regulated protein kinase ( ERK ) and p38 mitogen activated protein kinase
Balaraman et al., Biochem Biophys Res Commun 2004 : The use of inhibitors selective for ERK ( PD98059 ) and p38 ( SB203580 ) mitogen activated protein ( MAP ) kinase pathway showed that preincubation of cells with either SB203580 or PD98059 did not affect the binding activity of IRF-E, suggesting that both p38 and ERK MAP kinase activation are not necessary for IRF-E activation
Kim et al., J Immunol 2004 : TGF-beta1 and LY294002 suppressed LPS induced p38 mitogen activated kinase and c-Jun N-terminal kinase activity
Cuschieri et al., J Surg Res 2004 : LPS stimulation led to the mobilization of TLR4 to lipid rafts followed by phosphorylation and activation of IRAK, ERK 1/2, p38 , and JNK/SAPK
Ichikawa et al., Biol Pharm Bull 2004 : EGCG inhibited LPS induced phosphorylation of p38 mitogen activated protein kinase ( MAPK ), but not Jun N-terminal kinase (JNK), while EGCG augmented LPS induced phosphorylation of p44/p42 extracellular signal related kinase ( ERK )
Hou et al., J Biomed Sci 2006 (Brain Ischemia) : BT significantly reduced LPS induced NF-kappaB and p38 MAPK activation
Lin et al., Cell Signal 2007 : Consistently, LPS stimulated phosphorylation of p42/p44 MAPK and p38 was attenuated by pretreatment with U0126 or SB202190, and transfection with these siRNAs, respectively
West et al., J Trauma 2007 (Systemic Inflammatory Response Syndrome) : No basal Mono or PMN p38 was seen in healthy controls, but LPS significantly activated p38 in both cell types ... Both PMN and Mono from patients with SIRS had low basal but high LPS stimulated p38 , whereas p38 activation was impaired in patients with sepsis
Tsai et al., J Cell Biochem 2008 : Cilostazol significantly inhibited LPS induced activation of p38 , JNK, and nuclear factor-kappaB, and the respective inhibitors of p38 and JNK greatly reduced the level of LPS induced MCP-1 and MMP-9, suggesting the involvement of the p38 and JNK pathways
Brooks et al., Inflamm Res 2007 (Endotoxemia...) : In vivo, LPS stimulates TxA2 production and p38 MAPK phosphorylation in equine platelets and leukocytes at a concentration within a similar range to those reported in clinical endotoxaemia
Al-Hertani et al., Clin Invest Med 2007 : We show that p38 phosphorylation in newborn PMN is attenuated in response to LPS stimulation even though adult and newborn PMN have similar amounts of p38 protein
Ou et al., Respirology 2008 : However, LPS stimulated expression of p38 and ERK1/2 in airway epithelium was not affected by roxithromycin
Martins et al., Shock 2010 (Diabetes Mellitus, Experimental...) : Relative to control rats, diabetic rats exhibited a significant reduction in the LPS induced phosphorylation of extracellular signal regulated kinase ( 64 % ), p38 ( 70 % ), protein kinase B ( 67 % ), and protein kinase C alpha ( 57 % ) and delta ( 65 % ) and in the expression of iNOS ( 32 % ) and cyclooxygenase 2 ( 67 % ) in the lung homogenates
Noguchi et al., J Endod 2009 : We also found that LPS induced expression of COX-2, IL-6, and TNF-alpha and p38 activation were markedly suppressed when LPS was pretreated with ozonated water
Khuda et al., Immunology 2010 : Seladin-1 inhibited LPS induced activation of p38 but not nuclear factor-kappaB and inhibited the production of tumour necrosis factor-alpha in response to LPS
Hsieh et al., Phytomedicine 2011 (Bone Resorption...) : On osteoclasts, icariin suppresses LPS mediated activation of the p38 and JNK ; while on the osteoblasts, icariin reduced the LPS induced activation of ERK1/2 and I-kappa-B-alpha ( I?Ba ), but increased the activation of p38
Peirce et al., PloS one 2010 : Moreover, LPS induced activation of the MAP kinases ERK and p38 was enhanced in cells over expressing Themis2 whereas the activation of JNK, IRF3 or NF-kappaB p65, was unaffected
Cho et al., Mol Immunol 2011 : However, IL-4 did not affect LPS induced phosphorylation of ERK and p38
Kim et al., Evidence-based complementary and alternative medicine : eCAM 2012 : In addition, Myrrh inhibited LPS induced activation of c-jun NH ( 2 ) -terminal kinase ( JNK ) but not of extracellular signal regulated kinase ( ERK ), p38 , and nuclear factor-?B
Zhang et al., J Immunol 2012 (MAP Kinase Signaling System) : Moreover, in BMM from MKP1 ( -/- ) mice, the inhibition of LPS induced p38 phosphorylation by vitamin D was completely abolished
Figueroa et al., J Immunol 2012 : Cells transfected with D299G TLR4 exhibited impaired LPS induced phosphorylation of p38 and TANK binding kinase 1, activation of NF-?B and IFN regulatory factor 3, and induction of IL-8 and IFN-ß mRNA, whereas T399I TLR4 did not cause statistically significant inhibition
Herath et al., PloS one 2013 (MAP Kinase Signaling System) : In addition, LPS1690 induced significant expression of NF-?B and p38 MPAK pathways related genes, such as NFKBIA, NFKB1, IKBKB, MAP2K4 and MAPK8
Wu et al., Cell Res 2013 : Mlkl-deficient MEFs and macrophages were indistinguishable from wild-type cells in their ability to activate NF-?B, ERK, JNK, and p38 in response to TNF and lipopolysaccharides (LPS) , respectively
Schumann et al., Glia 1998 (Astrocytoma) : We show that LPS and PCW initiate tyrosine phosphorylation and activation of erk-1, erk-2, and p38 in a dose dependent fashion