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IRF6 — PTGS1

Text-mined interactions from Literome

Lo et al., J Surg Res 1999 : In comparison, COX-1 mRNA expression was not affected by either LPS stimulation or EPA incubation
Moon et al., Inflamm Res 1999 (Inflammation) : COX-1 and COX-2 protein and mRNA expression was determined by BMMC in the presence of KL, LPS and IL-10
Ermert et al., Am J Pathol 2000 : Both the Cox-1 mRNA, quantified in the whole lung homogenate, and the cellular localization of Cox-1 were unchanged in response to LPS
Clancy et al., J Immunol 2000 : In contrast, NO inhibited COX-2 derived PGE2 production in both LPS stimulated macrophages and COX-1 knockout cells
Berg et al., J Immunol 2001 : COX-1 protein levels were not affected by LPS stimulation in either wt or IL-10 ( -/- ) mice
Steiner et al., Neuroimmunomodulation 2001 (Fever) : COX-1 is not involved in intravenous LPS fever production, and COX-2 appears to play a greater role in the late than in the early phase of intravenous LPS fever in guinea pigs
Zamamiri-Davis et al., Free Radic Biol Med 2002 : In comparison, COX-1 protein expression was not affected by either LPS stimulation or Se status
Zhang et al., J Comp Neurol 2003 (Fever) : In contrast, the COX-1 inhibitor resulted in a profound hypothermic response to LPS and blocked LPS induced Fos-immunoreactivity in the PVH, PB, NTS, and VLM, although it had no effect on the VMPO
Jiang et al., Mol Cell Biochem 2003 : In this study, the effect of phorbol 12-myristate 13-acetate ( PMA ), tumor necrosis factor alpha (TNFalpha), lipopolysaccharide (LPS) and macrophage-colony stimulating factor ( M-CSF ) on AA release and prostaglandin E2 ( PGE2 ) production and the expression of cPLA2 and COX-1 and -2 were investigated in U937 human pre-monocytic cells and fully differentiated macrophages ... PMA induced COX-1 expression in U937 cells whereas LPS induced COX-2 expression in macrophages
Chen et al., J Cell Physiol 2003 : Both GSE and NAC resulted in significant exacerbation of the LPS stimulated increase in COX-2 gene and protein expression and prostaglandin release, and suppressed the LPS induced decrease in COX-1
Katagiri et al., Hepatology 2004 (Endotoxemia) : In addition, a selective COX-1 inhibitor, SC-560, a selective COX-2 inhibitor, NS-398, and indomethacin significantly attenuated hepatic responses to LPS including microcirculatory dysfunction and release of ALT and TNF alpha
Lappas et al., J Clin Endocrinol Metab 2004 : Treatment of placenta, amnion, and choriodecidua with SASP concentrations greater than 5 mM significantly inhibited basal and/or LPS stimulated type II PLA(2) content and release, 13,14-dihydro-15-keto PGF ( 2alpha ) release, and cPLA(2) protein content ( ANOVA, P < 0.05 ) ; however, no effect of SASP was observed on basal or LPS stimulated COX-1 or COX-2 protein
Inoue et al., J Appl Toxicol 2004 (Inflammation) : This study examined the effects of components of DEP on the lung expression of cyclooxygenase (COX)-1 and -2 in the presence or absence of LPS
Kis et al., Am J Physiol Regul Integr Comp Physiol 2005 : LPS stimulation increased the expression of COX-2 but not COX-1 or COX-3
West et al., Dig Dis Sci 2006 (Disease Models, Animal...) : LPS increased COX-2 but not COX-1 expression
Wu et al., Biol Pharm Bull 2007 : Furthermore, TET at 100 microM significantly blocked the LPS induction of iNOS and COX-2 expression, but not the COX-1
Yang et al., Neurol Res 2007 : The effects of amygdalin extracted from Armeniacae semen on the LPS stimulated mRNA expressions of cyclooxygenase (COX)-1 , COX-2 and inducible nitric oxide synthase (iNOS) in the mouse BV2 microglial cells were investigated using 3- ( 4,5-dimethylthiazol-2-yl ) -2,5-diphenyltetrazolium bromide ( MTT ) assay, reverse transcription-polymerase chain reaction ( RT-PCR )
Wu et al., Am J Chin Med 2007 : EAM at 100 mug/ml significantly blocked the LPS induction of iNOS and COX-2 expression, but not COX-1
Eckert et al., Vet Immunol Immunopathol 2007 : In contrast, LPS stimulation did not affect COX-1 protein expression
Font-Nieves et al., J Biol Chem 2012 : Induction of COX-2 enzyme and down-regulation of COX-1 expression by lipopolysaccharide (LPS) control prostaglandin E2 production in astrocytes ... In contrast, LPS down-regulated COX-1 in an MyD88 dependent fashion, and COX-1 deficiency increased PGE ( 2 ) production after LPS
Soliman et al., Lipids 2013 : In BV-2 microglia, we found that LPS increased the phosphorylation-state of cytosolic phospholipase A2 (cPLA2), reduced the levels of phospholipase C (PLC) ß1, and increased the levels of cyclooxygenase (Cox)-1 and -2 ... In primary astrocytes, LPS increased the phosphorylation of cPLA2 and increased the levels of Cox-1 and Cox-2
Noguchi et al., Inflammation 1996 (Periodontal Diseases) : Immunohistochemical staining of COX-2 protein demonstrated that expression of COX-2 protein was increased at 24 h after P gingivalis-LPS stimulation, while expression of COX-1 protein was not affected by P. gingivalis-LPS