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EGR1 — IRF6

Text-mined interactions from Literome

Guha et al., Blood 2001 (MAP Kinase Signaling System) : In contrast, PD98059 and dominant negative mutants of the Ras-Raf1-MEK-ERK ( extacellular signal regulated kinase ) pathway strongly inhibited LPS induction of Egr-1 expression ... In kinetic experiments LPS induction of Egr-1 expression preceded induction of TF expression ... It was demonstrated that LPS induction of the Egr-1 promoter was mediated by 3 SRE sites, which bound an LPS-inducible complex containing serum response factor and Elk-1 ... The data indicate that LPS induction of Egr-1 gene expression is required for maximal induction of the TNF-alpha and TF genes in human monocytic cells
Shi et al., Am J Physiol Cell Physiol 2002 : LPS rapidly increased early growth response factor (Egr)-1 binding to the TNF-alpha promoter ; this response was blunted in cells treated with PD-98059 or transfected with dominant negative ERK1/2 ... Using a chloramphenicol acetyltransferase reporter gene linked to the Egr-1 promoter, we show that LPS increased Egr-1 promoter activity via an ERK1/2 dependent mechanism
Kadl et al., Vascul Pharmacol 2002 (Inflammation) : We found that both OxPAPC and LPS induced expression of early growth response factor 1 (EGR-1) and monocyte chemoattractant protein 1 ( MCP-1 ) in HUVEC and of JE, the mouse homologue of MCP-1, in liver and heart
Pawlinski et al., Blood 2003 (Disease Models, Animal...) : In this study, the role of Egr-1 in lipopolysaccharide (LPS) induction of TF and inflammatory mediators in vivo was evaluated using Egr-1 ( +/+ ) and Egr-1 ( -/- ) mice
Mostecki et al., J Biol Chem 2005 : Chromatin immunoprecipitation experiments confirm LPS induced binding of Egr-1 to the SOCS-1 promoter in vivo
McMullen et al., Gastroenterology 2005 (Disease Models, Animal...) : These data show that Egr-1 contributes to increased LPS mediated TNF-alpha expression after chronic ethanol and that the absence of Egr-1 prevents chronic ethanol induced fatty liver, as well as increased sensitivity to LPS
Molor-Erdene et al., Thromb Haemost 2005 : Although activation of nuclear factor-kappaB (NF-kappaB), activator protein-1 (AP-1) and extracellular signal regulated kinase ( ERK ) 1/2 were shown to be critically involved in LPS induced increases in TF activities in isolated monocytes, UTI inhibited phosphorylation of ERK1/2 and decreased expression of early growth response factor-1 (Egr-1) induced by LPS without affecting the activation of NF-kappaB and AP-1
Thakur et al., Am J Physiol Gastrointest Liver Physiol 2006 : gAcrp also normalized LPS stimulated DNA binding activity of early growth response-1 with greater sensitivity in Kupffer cells from rats fed chronic ethanol
Zhou et al., Acta Pharmacol Sin 2007 : In a concentration dependent manner, 1,8-Cineol reduces LPS induced Egr-1 expression in nuclei and in whole cell of THP-1 cells, but shows no effect on NF-kappaB expression
Berchtold et al., BMC immunology 2008 : By using stably transfected RAW264.7 macrophages overexpressing IFIT-2 we found that IFIT-2 inhibits selectively LPS induced expression of TNF-alpha, IL-6, and MIP-2 but not of IFIT-1 or EGR-1
Díaz-Muñoz et al., Cell Signal 2010 : Furthermore, LPS induced the expression of Egr-1 that cooperated with NF-kappaB in the up-regulation of COX-2 and mPGES-1
Gorina et al., Glia 2011 : p38 exerted a strong influence on LPS induced gene expression by regulating the phosphorylation of Stat1 and the transcriptional activity of NF?B, while JNK regulated the Jak1/Stat1 pathway, and ERK1/2 controlled the expression of Egr-1 and influenced MyD88 dependent MMP-9 expression
Haschemi et al., PloS one 2011 (Inflammation) : Ectopic expression of a SUMOylation-defective PPAR?-K365R mutant partially abolished CO-mediated suppression of LPS induced Egr-1 promoter activity
Shoeb et al., Free Radic Biol Med 2012 (Inflammation) : Furthermore, benfotiamine prevented the LPS induced phosphorylation of ERK1/2 and expression of transcription factors NF-?B and Egr-1
Groupp et al., J Biol Chem 1996 : These data suggest that LPS stimulation of THP-1 cells activates binding of c-Jun, Ets, and Egr-1 to the TF promoter and implicates these factors in the transcriptional activation of TF mRNA synthesis
Yao et al., J Biol Chem 1997 : In addition, LPS stimulation induced the binding of cognate nuclear factors to the Egr-1 and kappaB3 sites, which were identified as Egr-1 and p50/p65, respectively
Pendurthi et al., Arterioscler Thromb Vasc Biol 1997 : The present studies are the first to demonstrate that PMA, but not LPS , TNF alpha, and thrombin, induced Egr-1 binding to the second serum-responsive region ( SRR-2 ) of TF promoter and that curcumin inhibited the PMA induced Egr-1 binding to SRR-2