PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 22366248-9 2012 NOSH-aspirin inhibited ovine COX-1 more than ovine COX-2. Aspirin 5-12 cytochrome c oxidase I, mitochondrial Mus musculus 29-34 25591798-8 2015 RESULTS: In Western blot analysis, COX-1 expression levels were found to be significantly reduced in mice treated with 3-(5-chlorofuran-2-yl)-5-methyl-4-phenylisoxazole (P6) in comparison to mice pretreated with aspirin (ASA), which exhibited higher levels of COX-1, thus confirming the high selectivity of P6 towards COX-1 enzyme inhibition. Aspirin 212-219 cytochrome c oxidase I, mitochondrial Mus musculus 35-40 25591798-8 2015 RESULTS: In Western blot analysis, COX-1 expression levels were found to be significantly reduced in mice treated with 3-(5-chlorofuran-2-yl)-5-methyl-4-phenylisoxazole (P6) in comparison to mice pretreated with aspirin (ASA), which exhibited higher levels of COX-1, thus confirming the high selectivity of P6 towards COX-1 enzyme inhibition. Aspirin 221-224 cytochrome c oxidase I, mitochondrial Mus musculus 35-40 23240590-2 2013 Aspirin, a non-steroidal anti-inflammatory drug, simultaneously inhibits the aromatase activity of COX-1 and COX-2 isoforms, which is needed for prostaglandin synthesis. Aspirin 0-7 cytochrome c oxidase I, mitochondrial Mus musculus 99-104 16614756-5 2006 These responses were attenuated by COX-1 knock down, which mimics the beneficial effects of low-dose aspirin. Aspirin 101-108 cytochrome c oxidase I, mitochondrial Mus musculus 35-40 16326168-7 2006 At the end of the study, LDLR(-/-) mice that had received aspirin had suppressed biosynthesis of thromboxane B2, the major products of COX-1 activity, reduced monocyte chemoattractant protein-1, and soluble intercellular adhesion molecule-1 levels compared with controls. Aspirin 58-65 cytochrome c oxidase I, mitochondrial Mus musculus 135-140 14592546-2 2003 It is possible that inhibition of cyclooxygenase (COX)-1 is the major action of aspirin involved in its analgesic and antipyretic effects, and inhibition of COX-2 is responsible for its anti-inflammatory action. Aspirin 80-87 cytochrome c oxidase I, mitochondrial Mus musculus 34-56 14592546-5 2003 The antipyretic action of aspirin may be mediated by inhibition of COX-3 in hypothalamic endothelial cells or by inhibition of COX-1 localised close to sensory receptors of peripheral vagal afferents. Aspirin 26-33 cytochrome c oxidase I, mitochondrial Mus musculus 127-132 9535546-3 1998 Aspirin, more selective in vitro for the inhibition of COX-1 (10,200 (mg/kg) and nimesulide, a selective in vitro inhibitor of COX-2 (0.5, 5 mg/kg) were dosed p.o. Aspirin 0-7 cytochrome c oxidase I, mitochondrial Mus musculus 55-60 11745453-1 2001 The epidemiologic evidence and rodent studies suggest strongly that nonselective inhibitors of cyclooxygenase (COX) enzymes such as aspirin, inhibiting both COX-1 and COX-2 isoforms, reduce the incidence of and mortality from intestinal tumors. Aspirin 132-139 cytochrome c oxidase I, mitochondrial Mus musculus 157-162 11457426-3 2001 In primary cortical neurons, both indomethacin (COX-1/-2 nonselective inhibitor) and aspirin (COX-1 preferential inhibitor) reduced basal and kainic acid-induced PGE(2) production significantly and prevented neuronal cell death after kainic acid treatment. Aspirin 85-92 cytochrome c oxidase I, mitochondrial Mus musculus 94-99 11195467-3 2000 The NSAIDs used in this study include acetylsalicylic acid (ASA) that is anti-inflammatory with COX-1 and COX-2 inhibition and N-[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide (NS398) that is a specific COX-2 inhibitor. Aspirin 38-58 cytochrome c oxidase I, mitochondrial Mus musculus 96-101 11195467-3 2000 The NSAIDs used in this study include acetylsalicylic acid (ASA) that is anti-inflammatory with COX-1 and COX-2 inhibition and N-[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide (NS398) that is a specific COX-2 inhibitor. Aspirin 60-63 cytochrome c oxidase I, mitochondrial Mus musculus 96-101 10692466-2 2000 The two isoforms of cyclooxygenase, COX-1 and COX-2, are acetylated by aspirin at Ser-530 and Ser-516, respectively, in the cyclooxygenase active site. Aspirin 71-78 cytochrome c oxidase I, mitochondrial Mus musculus 36-41 10692466-6 2000 Site-directed mutagenesis of Val-434, Arg-513, and Val-523 in mouse COX-2 to their COX-1 equivalents resulted in abrogation of 11- and 15-HETE production after aspirin treatment, confirming the hypothesis that these residues are the major isoform selectivity determinants regulating HETE production. Aspirin 160-167 cytochrome c oxidase I, mitochondrial Mus musculus 83-88 10339595-1 1999 The antiinflammatory action of aspirin generally has been attributed to direct inhibition of cyclooxygenases (COX-1 and COX-2), but additional mechanisms are likely at work. Aspirin 31-38 cytochrome c oxidase I, mitochondrial Mus musculus 110-115 11964481-2 2002 Aspirin affords cardioprotection through inhibition of TxA2 formation by platelet cyclooxygenase (COX-1). Aspirin 0-7 cytochrome c oxidase I, mitochondrial Mus musculus 98-103 11180504-1 2001 To study the possible role of the isoenzymes of cyclooxygenase COX-1 and COX-2 in the MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) mouse model of Parkinson"s disease we used acetylsalicylic acid, a COX-1/COX-2 inhibitor, in comparison with meloxicam, a preferential COX-2 inhibitor. Aspirin 181-201 cytochrome c oxidase I, mitochondrial Mus musculus 63-68 11180504-12 2001 In conclusion, the inhibition of either COX-1/COX-2 by acetylsalicylic acid or preferentially COX-2 by meloxicam provided a clear neuroprotection against MPTP-toxicity on the striatal and nigral levels. Aspirin 55-75 cytochrome c oxidase I, mitochondrial Mus musculus 40-45 10970676-9 2000 Pretreatment of the mice with aspirin, an irreversible inhibitor of COX1 and COX2, prevented the hypophagic response to IL-1, 16 h, but not 40 h later. Aspirin 30-37 cytochrome c oxidase I, mitochondrial Mus musculus 68-72 9850065-15 1998 Anti-COX-1 and -2, arachidonic acid, ASA, and NS-398 inhibited NNK bioactivation by COX-1 and -2 from 22-49%. Aspirin 37-40 cytochrome c oxidase I, mitochondrial Mus musculus 84-96 9535546-13 1998 CONCLUSION: In this model of chronic inflammation, aspirin, more selective for the inhibition of COX-1 is more effective than the selective COX-2 inhibitors nimesulide and NS-398 at inhibiting granuloma dry weight, vascularity and COX activity. Aspirin 51-58 cytochrome c oxidase I, mitochondrial Mus musculus 97-102 27074574-6 2016 Platelet COX-1 inhibition by aspirin administration to mice prevented the increased rate of metastasis as well as the enhanced production of TXA2 and PGE2 induced by the in vitro priming of HT29 cells by platelets. Aspirin 29-36 cytochrome c oxidase I, mitochondrial Mus musculus 9-14 31442897-3 2019 Expected inhibition of COX1 by ASA was ascertained by a strong decrease in TXB2 production, and its effect on platelet function and hemostasis, by decreased collagen-induced aggregation and increased bleeding time, respectively. Aspirin 31-34 cytochrome c oxidase I, mitochondrial Mus musculus 23-27 31469551-6 2019 Substitution of Arg-513 with histidine (the equivalent residue in COX-1) resulted in a 2-fold potentiation of aspirin inhibition, in support of the hypothesis that the presence of histidine in COX-1 lowers the activation barrier associated with the formation of the initial noncovalent enzyme-inhibitor complex. Aspirin 110-117 cytochrome c oxidase I, mitochondrial Mus musculus 66-71 31469551-6 2019 Substitution of Arg-513 with histidine (the equivalent residue in COX-1) resulted in a 2-fold potentiation of aspirin inhibition, in support of the hypothesis that the presence of histidine in COX-1 lowers the activation barrier associated with the formation of the initial noncovalent enzyme-inhibitor complex. Aspirin 110-117 cytochrome c oxidase I, mitochondrial Mus musculus 193-198 34182131-4 2021 The contribution of platelet TXA2 biosynthesis on enhanced blood pressure (BP) and overload-induced cardiac fibrosis was explored in mice by treating with low-dose Aspirin, resulting in selective inhibition of platelet cyclooxygenase (COX)-1-dependent TXA2 generation. Aspirin 164-171 cytochrome c oxidase I, mitochondrial Mus musculus 219-241 32592197-1 2020 Aspirin prevents thrombosis by inhibiting platelet cyclooxygenase (COX)-1 activity and the production of thromboxane (Tx)A2 , a pro-thrombotic eicosanoid. Aspirin 0-7 cytochrome c oxidase I, mitochondrial Mus musculus 51-73 32251451-9 2020 Analysis of eicosanoids in stirred blood demonstrated that administration of ASA at a dose of 12 mg kg-1 to cancer-bearing mice had an effect beyond inhibition of platelet COX-1, suggesting long-term treatment with low-dose aspirin is not a selective murine platelet COX-1/TXA2 pathway inhibitor in cancer-bearing mice. Aspirin 77-80 cytochrome c oxidase I, mitochondrial Mus musculus 172-177 32251451-9 2020 Analysis of eicosanoids in stirred blood demonstrated that administration of ASA at a dose of 12 mg kg-1 to cancer-bearing mice had an effect beyond inhibition of platelet COX-1, suggesting long-term treatment with low-dose aspirin is not a selective murine platelet COX-1/TXA2 pathway inhibitor in cancer-bearing mice. Aspirin 77-80 cytochrome c oxidase I, mitochondrial Mus musculus 267-272 30017554-0 2019 COX-1 mediates IL-33-induced extracellular signal-regulated kinase activation in mast cells: Implications for aspirin sensitivity. Aspirin 110-117 cytochrome c oxidase I, mitochondrial Mus musculus 0-5 27998883-2 2017 In this study, using colon cancer as an example, we provide both in vitro (cell culture) and in vivo (chemically induced mouse model of colon cancer) evidence that this profound antineoplastic action may be associated with aspirin"s ability to irreversibly inhibit COX-1-mediated platelet activation, thereby blocking platelet-cancer cell interactions, which promote cancer cell number and invasive potential. Aspirin 223-230 cytochrome c oxidase I, mitochondrial Mus musculus 265-270