◀ Back to IRF6

CRK — IRF6

Text-mined interactions from Literome

Hippenstiel et al., Blood 2000 : Specific inactivation of RhoA/Cdc42/Rac1 by Clostridium difficile toxin B-10463 ( TcdB-10463 ) reduced LPS induced tyrosine phosphorylation, nuclear factor (NF)-kappaB dependent gene expression, IL-8 messenger RNA, and IL-8 protein accumulation but showed no effect on LPS dependent p38 MAPK activation
Uchimura et al., Hepatology 2001 : PPAR gamma:RXR activation did not affect the level of LPS induced phosphorylation of c-jun N-terminal kinase and p38 mitogen activated protein kinase
Darveau et al., Infect Immun 2002 : In contrast, no p38 MAP kinase activation was observed in response to P. gingivalis LPS in human endothelial cells or CHO cells transfected with human Toll-like receptor 4 (TLR-4) ... In addition, P. gingivalis LPS was an effective inhibitor of Escherichia coli induced p38 MAP kinase phosphorylation in both endothelial cells and CHO cells transfected with human TLR-4
Bozinovski et al., J Biol Chem 2002 (MAP Kinase Signaling System) : These data implicate GM-CSF dependent activation of Akt in the amplification of this response and demonstrate the role of Erks rather than p38 in lung LPS inflammatory responses
Pinteaux et al., J Neurochem 2002 : Bacterial lipopolysaccharide (LPS) caused increased expression of IL-1RI, IL-1RII and IL-1RAcP mRNAs, induced the release of IL-1beta, IL-6 and prostaglandin-E2 ( PGE2 ), and activated nuclear factor kappaB (NF-kappaB) and the mitogen activated protein kinases ( MAPKs ) p38 , and extracellular signal regulated protein kinase ( ERK1/2 ), but not c-Jun N-terminal kinase (JNK) in microglial cultures
Malcolm et al., J Biol Chem 2003 : LPS , but not IFNalpha, substantially activated p38
Abraham et al., J Immunol 2003 (Acute Disease) : There was no effect of uPA on LPS induced activation of p38 mitogen activated protein kinase in neutrophils
Khadaroo et al., Surgery 2003 : The Src inhibitor, PP2, prevented only the LPS induced earlier phosphorylation after oxidant stress and had no effect on LPS activation of p38 alone
Matsuyama et al., J Immunol 2003 (MAP Kinase Signaling System) : Activation of DDR1 on immature DCs resulted in their partial maturation ; however, DDR1 activation markedly amplified TNF-alpha- and LPS induced phenotypic and functional maturation of DCs through activation of p38 mitogen activated protein kinase ( MAPK ), suggesting the involvement of DDR1b in this process
Kojima et al., Am J Physiol Gastrointest Liver Physiol 2004 (MAP Kinase Signaling System) : Whereas LPS stimulated both the p38 and ERK1/2 but not the stress activated protein kinase/c-Jun NH ( 2 ) -terminal kinase, signaling pathways in the YAMC cells, all three were stimulated in RAW macrophage cells ( in which no LPS induced HSP25 expression was observed )
Nishiki et al., Am J Physiol Cell Physiol 2004 (MAP Kinase Signaling System) : G-CSF did not affect LPS induced activation of ERK, p38 , JNK, and NF-kappa B, indicating that G-CSF affects the pathway downstream or independently of these signaling molecules
Ho et al., Br J Pharmacol 2004 (Inflammation) : Our data clearly indicated an inhibition ( IC ( 50 ) =1.7 microm ) of LPS mediated p38 MAPK activity, but not of extracellular signal regulated kinase ( ERK ) or c-Jun N-terminal kinase (JNK) activity
Woo et al., J Immunol 2004 : LPS induced MMP-9 expression and p38 kinase phosphorylation were also inhibited by rotenone, a specific inhibitor of mitochondrial complex I, supporting the role of mitochondrial ROS in LPS signaling to MMP-9
An et al., Blood 2005 (Inflammation) : Neither disrupting phosphatase activity nor using the PI-3K pathway inhibitor LY294002 or wortmannin could significantly block SHIP1 mediated inhibition of LPS induced ERK1/2, p38 , and JNK activation and TNF-alpha production, demonstrating that SHIP1 inhibits LPS induced activation of MAPKs and cytokine production primarily by a phosphatase activity- and PI-3K independent mechanism
Kim et al., Immunopharmacol Immunotoxicol 2005 : Mercury modulates LPS induced p38 and ERK activation and downstream TNFalpha and IL-6 expression in mouse liver
Maung et al., J Leukoc Biol 2005 (Burns) : However, with the use of antibodies specific for the phosphorylated ( activated ) forms of the three MAPKs, we found that macrophages from burn mice showed a twofold increase in purified lipopolysaccharide (LPS) stimulated p38 activation as compared with cells from sham mice on days 1 and 7 post-injury, whereas ERK and SAPK/JNK activation was increased by burn injury only on day 1
Tsao et al., Biochem Pharmacol 2005 : HPB had no effect on the LPS induced phosphorylation of extracellular signal regulated kinase ( ERK ), p38 mitogen activated protein kinases ( MAPK ), and c-Jun NH ( 2 ) -terminal kinase ( JNK )
Cherla et al., J Leukoc Biol 2006 (MAP Kinase Signaling System) : We show that treatment of differentiated THP-1 cells with purified Stx1 resulted in prolonged activation of c-Jun N-terminal kinase (JNK) and p38 mitogen activated protein kinase ( MAPK ) cascades, and lipopolysaccharides (LPS) rapidly triggered transient activation of JNK and p38 and prolonged activation of extracellular signal regulated kinase cascades
Grishin et al., J Immunol 2006 (Disease Models, Animal...) : LPS increased COX-2 and activating phosphorylation of p38 with similar dose-response
Hsu et al., Mol Pharmacol 2007 : In addition, Hsp90 is important for IL-1 protein translation, plays a minor role in IL-1 mRNA transcription, and is involved in nuclear factor-kappaB activation and the phosphorylation and activation of p38, c-Jun NH2-terminal kinase, and extracellular signal regulated kinase ; however, Hsp90 plays a more important role in LPS stimulated p38 activation
Jin et al., J Cell Biochem 2007 (Muscular Atrophy) : LPS activated p38 and NF-kappaB, while inhibiting AKT ; whereas, curcumin administration inhibited LPS stimulated p38 activation, without altering the effect of LPS on NF-kappaB and AKT
Tanaka et al., Neurosci Lett 2008 : In primary glial cultures, LPS increased the phosphorylation levels of c-Jun amino-terminal kinase 1 (JNK1) and p38 mitogen activated protein kinase ( MAPK ) ; in primary microglial cultures, it enhanced phosphorylation of extracellular signal regulated kinase ( Erk )
Bhatia et al., Arch Biochem Biophys 2008 : However, mangiferin did not modify LPS mediated phosphorylation of p38 mitogen activated protein kinase ( p38 MAPK ), a key factor involved in enhancing COX-2 mRNA stability and COX-2 translation in primary microglia
El-Remessy et al., Molecular vision 2008 (Uveitis) : At a later phase, LPS induced NO, ROS, and p38 MAPK activation that peaked at 2-6 h and was accompanied by morphological change of microglia
Noman et al., Innate Immun 2009 : Thalidomide prevented the activation of nuclear factor (NF)-KB by down regulating phosphorylation of inhibitory KB factor ( IKB ), and IKB kinase (IKK)-alpha and IKK-beta Moreover, thalidomide inhibited LPS induced phosphorylation of AKT, p38 and stress activated protein kinase ( SAPK ) /JNK
Xing et al., Microvasc Res 2010 (Inflammation) : Both LPS and TNFalpha caused sustained activation of p38 and ERK1/2 MAP kinases, increased phosphorylation and degradation of negative regulator of NFkappaB signaling IkBalpha, and increased Rho-kinase mediated phosphorylation of myosin phosphatase MYPT1 leading to accumulation of phosphorylated myosin light chains
Kuo et al., Inflammation 2010 : PGI ( 2 ) analogues enhanced LPS induced phospho-p38 expression
Cao et al., Int Immunopharmacol 2010 (Disease Models, Animal...) : We further observed that MA prevented the LPS induced nuclear factor-kappa B (NF-kappaB) translocation from the cytoplasm into the nucleus, and inhibited the LPS induced phosphorylation of extracellular signal regulated kinase 1/2 ( ERK1/2 ) and p38
Sarkar et al., Mol Cell Biol 2011 : Indeed, knockdown of AUF1 impairs LPS mediated p38 mitogen activated protein kinase ( MAPK ) and NF-?B signaling, and the expression of an RNA interference-refractory p40 ( AUF1 ) cDNA restores both signaling pathways
Zhao et al., Am J Respir Cell Mol Biol 2011 (Acute Lung Injury...) : Moreover, down-regulation of S1PL expression by short interfering RNA ( siRNA ) in primary human lung microvascular endothelial cells increased S1P levels, and attenuated LPS mediated phosphorylation of p38 mitogen activated protein kinase and I-?B, IL-6 secretion, and endothelial barrier disruption via Rac1 activation
Watanabe et al., Biochem Biophys Res Commun 2011 : Notably, the extract enhanced LPS induced phosphorylation of p38 mitogen activated protein kinase ( MAPK ), while it suppressed LPS induced phosphorylation of c-Jun N-terminal kinase (JNK) MAPK
Barona et al., J Pharm Pharmacol 2011 : These results suggest that the effect of LPS on ACh induced contractions in the rabbit duodenum might be mediated by TLR4 and p38 , JNK1/2 and MEK1/2 MAPKs
Noh et al., Exp Cell Res 2011 (Breast Neoplasms...) : Apoptosis signal regulating kinase 1 ( ASK1 ) is also required for LPS induced activation of p38 , which is a crucial determinant for the production of pro-inflammatory cytokines via Toll-like receptor 4 (TLR4) in endotoxemia
Scott et al., J Biol Chem 2011 (MAP Kinase Signaling System) : Activation of p38 was redox-sensitive as H(2)O ( 2 ) caused p38 phosphorylation, and ROS scavenging significantly reduced LPS induced phospho-p38 expression
Fiebich et al., Phytother Res 2012 (MAP Kinase Signaling System) : The extract had no effect on the LPS induced binding of nuclear factor-?B in RAW 264.7 cells, on LPS induced degradation of I?Ba or on LPS induced activation of mitogen activated protein kinases ( MAPK ), p38MAPK and JNK in human monocytes
Egorina et al., Thromb Res 2012 (MAP Kinase Signaling System) : Similarly, LPS induced increase in levels of phosphorylated Erk1/2, p38 , and JNK was markedly diminished by BMP-2 pretreatment
Zhang et al., J Immunol 2012 (MAP Kinase Signaling System) : In conclusion, this study identified the upregulation of MKP-1 by vitamin D as a novel pathway by which vitamin D inhibits LPS induced p38 activation and cytokine production in monocytes/macrophages
Mizunoe et al., J Pharmacol Sci 2012 (Cystic Fibrosis) : Notably, despite the induction of nuclear factor-?B and MAP kinases during TLR2 or TLR4 activation in CFBE41o-, IL-17A dependent synergism appears to be the result of enhanced PGN- or LPS induced phosphorylation of p38
Kim et al., PloS one 2012 (Encephalitis) : In LPS-responsive HEK293T cells, overexpression of the human LRRK2 pathologic, kinase-active mutant G2019S increased basal and LPS induced levels of phosphorylated p38 and JNK, whereas wild-type and other pathologic ( R1441C and G2385R ) or artificial kinase-dead ( D1994A ) LRRK2 mutants either enhanced or did not change basal and LPS induced p38 and JNK phosphorylation levels
Byun et al., Biochem Biophys Res Commun 2012 (Inflammation) : In addition, EGCG treated DCs inhibited lipopolysaccharide (LPS) induced production of pro-inflammatory cytokines ( tumor necrosis factor [TNF ] -a, interleukin [ IL]-1ß, and IL-6 ) and activation of mitogen activated protein kinases ( MAPKs ), e.g., extracellular signal regulated kinase 1/2 ( ERK1/2 ), p38 , c-Jun N-terminal kinase (JNK), and nuclear factor ?B ( NF-?B ) p65 translocation through 67LR
Leow-Dyke et al., Journal of neuroinflammation 2012 (Immune System Diseases...) : In glial cultures, LPS induced activation of ERK1/2, p38 and JNK
Wang et al., J Nutr Biochem 2013 : In contrast, COX-2 appears to be regulated by p38 MAPK in RAW cells, but ?-TE has no effect on LPS stimulated p38 phosphorylation
Dauphinee et al., J Immunol 2013 (MAP Kinase Signaling System) : This interaction fosters ubiquitination of TRAF6 and TAK1 and promotes LPS induced NF-?B, JNK, and p38 activation, culminating in increased production of proinflammatory cytokines and increased LPS induced endothelial migration
Oh et al., Molecules (Basel, Switzerland) 2013 (Inflammation...) : The extract also had no effect on LPS stimulated p38 MAPK, JNK, and c-Jun phosphorylation, whereas ERK1/2 phosphorylation was strongly inhibited by BOWE