PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27712766-1 2016 Aspirin-exacerbated respiratory disease (AERD) involves overexpression of proinflammatory mediators, including 5-lipoxygenase and leukotriene C4 synthase (LTC4S), resulting in constitutive overproduction of cysteinyl leukotrienes. Aspirin 0-7 arachidonate 5-lipoxygenase Homo sapiens 111-125 27888917-2 2017 The hallmark of the disease is baseline overproduction of cysteinyl leukotrienes via the 5-lipoxygenase pathway, exacerbated by ingestion of aspirin. Aspirin 141-148 arachidonate 5-lipoxygenase Homo sapiens 89-103 33975019-3 2021 The treatment with ASA caused an increase in the gene expression of COX2 and ABCB1 in both MDR cell lines, and a decrease in the expression of ALOX5 in the FEPS cells. Aspirin 19-22 arachidonate 5-lipoxygenase Homo sapiens 143-148 25590316-1 2015 BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) is explained in part by overexpression of 5-lipoxygenase and leukotriene C4 synthase (LTC4S), resulting in constitutive overproduction of cysteinyl leukotrienes (CysLTs) and driving the surge in CysLT production that occurs with aspirin ingestion. Aspirin 12-19 arachidonate 5-lipoxygenase Homo sapiens 101-115 26678823-8 2016 ALOX5 was a common predictor of studies on NAR to both aspirin and NSAIDs. Aspirin 55-62 arachidonate 5-lipoxygenase Homo sapiens 0-5 25590316-1 2015 BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) is explained in part by overexpression of 5-lipoxygenase and leukotriene C4 synthase (LTC4S), resulting in constitutive overproduction of cysteinyl leukotrienes (CysLTs) and driving the surge in CysLT production that occurs with aspirin ingestion. Aspirin 288-295 arachidonate 5-lipoxygenase Homo sapiens 101-115 21712098-9 2011 The biosynthesis and formation of both 18S and 18R-series are enhanced with aspirin treatment and involve the utilization of dietary EPA as well as recombinant human 5-lipoxygenase and LTA(4) hydrolase in their stereospecific biosynthesis. Aspirin 76-83 arachidonate 5-lipoxygenase Homo sapiens 166-180 22262978-1 2012 Aspirin-exacerbated respiratory disease (AERD) is explained in part by over-expression of 5-lipoxygenase, leukotriene C4 synthase (LTC(4)S) and the cysteinyl leukotriene (CysLT) receptors (CysLT1 and 2), resulting in constitutive over-production of CysLTs and the hyperresponsiveness to CysLTs that occurs with aspirin ingestion. Aspirin 0-7 arachidonate 5-lipoxygenase Homo sapiens 90-104 22262978-1 2012 Aspirin-exacerbated respiratory disease (AERD) is explained in part by over-expression of 5-lipoxygenase, leukotriene C4 synthase (LTC(4)S) and the cysteinyl leukotriene (CysLT) receptors (CysLT1 and 2), resulting in constitutive over-production of CysLTs and the hyperresponsiveness to CysLTs that occurs with aspirin ingestion. Aspirin 311-318 arachidonate 5-lipoxygenase Homo sapiens 90-104 22095955-0 2012 Aspirin analogues as dual cyclooxygenase-2/5-lipoxygenase inhibitors: synthesis, nitric oxide release, molecular modeling, and biological evaluation as anti-inflammatory agents. Aspirin 0-7 arachidonate 5-lipoxygenase Homo sapiens 43-57 16825866-8 2006 SUMMARY: The HLA alleles DRB11302 and DQB10609, and the ALOX5 and FcepsilonRIalpha promoter polymorphisms, may contribute to the pathogenesis of aspirin-induced urticaria/angioedema. Aspirin 145-152 arachidonate 5-lipoxygenase Homo sapiens 56-61 15876305-0 2005 Polymorphism of tandem repeat in promoter of 5-lipoxygenase in ASA-intolerant asthma: a positive association with airway hyperresponsiveness. Aspirin 63-66 arachidonate 5-lipoxygenase Homo sapiens 45-59 16361798-9 2005 These results suggested that ALOX5 has a differing contribution in two major clinical pathogenesis related to ASA-sensitivity. Aspirin 110-113 arachidonate 5-lipoxygenase Homo sapiens 29-34 16583357-1 2006 In aspirin-intolerant subjects, adverse bronchial and nasal reactions to cyclooxygenase (COX) inhibitors are associated with over-production of cysteinyl-leukotrienes (cys-LTs) generated by the 5-lipoxygenase (5-LO) pathway. Aspirin 3-10 arachidonate 5-lipoxygenase Homo sapiens 194-208 15876305-1 2005 BACKGROUND: 5-Lipooxygenase (ALOX5) and 5-lipoxygenase-activating protein (ALOX5AP) are known as key enzymes in cysteinyl-leukotriene (cys-LT) production, critical mediators in aspirin acetylsalicyclic acid (ASA)-intolerant asthma (AIA). Aspirin 177-184 arachidonate 5-lipoxygenase Homo sapiens 29-34 15876305-1 2005 BACKGROUND: 5-Lipooxygenase (ALOX5) and 5-lipoxygenase-activating protein (ALOX5AP) are known as key enzymes in cysteinyl-leukotriene (cys-LT) production, critical mediators in aspirin acetylsalicyclic acid (ASA)-intolerant asthma (AIA). Aspirin 177-184 arachidonate 5-lipoxygenase Homo sapiens 40-54 15876305-1 2005 BACKGROUND: 5-Lipooxygenase (ALOX5) and 5-lipoxygenase-activating protein (ALOX5AP) are known as key enzymes in cysteinyl-leukotriene (cys-LT) production, critical mediators in aspirin acetylsalicyclic acid (ASA)-intolerant asthma (AIA). Aspirin 185-206 arachidonate 5-lipoxygenase Homo sapiens 29-34 15876305-1 2005 BACKGROUND: 5-Lipooxygenase (ALOX5) and 5-lipoxygenase-activating protein (ALOX5AP) are known as key enzymes in cysteinyl-leukotriene (cys-LT) production, critical mediators in aspirin acetylsalicyclic acid (ASA)-intolerant asthma (AIA). Aspirin 185-206 arachidonate 5-lipoxygenase Homo sapiens 40-54 15876305-1 2005 BACKGROUND: 5-Lipooxygenase (ALOX5) and 5-lipoxygenase-activating protein (ALOX5AP) are known as key enzymes in cysteinyl-leukotriene (cys-LT) production, critical mediators in aspirin acetylsalicyclic acid (ASA)-intolerant asthma (AIA). Aspirin 208-211 arachidonate 5-lipoxygenase Homo sapiens 29-34 15876305-1 2005 BACKGROUND: 5-Lipooxygenase (ALOX5) and 5-lipoxygenase-activating protein (ALOX5AP) are known as key enzymes in cysteinyl-leukotriene (cys-LT) production, critical mediators in aspirin acetylsalicyclic acid (ASA)-intolerant asthma (AIA). Aspirin 208-211 arachidonate 5-lipoxygenase Homo sapiens 40-54 10923603-2 2000 It was therefore logical to assume that an inhibitor of 5-lipoxygenase (5-LO), such as zileuton, given before and during oral challenges with ASA, might prevent ASA-induced respiratory reactions. Aspirin 142-145 arachidonate 5-lipoxygenase Homo sapiens 56-70 12890715-0 2003 Evidence that 5-lipoxygenase and acetylated cyclooxygenase 2-derived eicosanoids regulate leukocyte-endothelial adherence in response to aspirin. Aspirin 137-144 arachidonate 5-lipoxygenase Homo sapiens 14-28 11476469-8 2001 CONCLUSIONS: Our results indicated that aspirin-induced asthma is associated with overproduction of LT with a shift to the 5-lipoxygenase series of the arachidonate cascade and that leukotriene receptor antagonist are useful for AIA through inhibition of production of LT and eosinophilic inflammation in the airway. Aspirin 40-47 arachidonate 5-lipoxygenase Homo sapiens 123-137 10923603-2 2000 It was therefore logical to assume that an inhibitor of 5-lipoxygenase (5-LO), such as zileuton, given before and during oral challenges with ASA, might prevent ASA-induced respiratory reactions. Aspirin 161-164 arachidonate 5-lipoxygenase Homo sapiens 56-70 8898374-2 1996 We recently showed that ASA triggers the formation of a new series of potent bioactive eicosanoids, 15-epi-lipoxins (15-epi-LXs or ASA-triggered LX [ATL]), during interactions between prostaglandin endoperoxide synthase-2 (PGHS-2) in endothelial cells and 5-lipoxygenase (LO) in leukocytes. Aspirin 24-27 arachidonate 5-lipoxygenase Homo sapiens 256-270 9563738-0 1998 Benefits from adding the 5-lipoxygenase inhibitor zileuton to conventional therapy in aspirin-intolerant asthmatics. Aspirin 86-93 arachidonate 5-lipoxygenase Homo sapiens 25-39 9017785-4 1997 Both the 5-lipoxygenase inhibitors and the cysLT receptor antagonists have thus far demonstrated the capacity to improve pulmonary function and reduce symptoms in clinical models of asthma, such as exercise-, aspirin-, or antigen-induced bronchoconstriction, and to improve pulmonary function in patients with mild-to-moderate, chronic stable asthma. Aspirin 209-216 arachidonate 5-lipoxygenase Homo sapiens 9-23 8898374-2 1996 We recently showed that ASA triggers the formation of a new series of potent bioactive eicosanoids, 15-epi-lipoxins (15-epi-LXs or ASA-triggered LX [ATL]), during interactions between prostaglandin endoperoxide synthase-2 (PGHS-2) in endothelial cells and 5-lipoxygenase (LO) in leukocytes. Aspirin 131-134 arachidonate 5-lipoxygenase Homo sapiens 256-270 8658372-7 1996 RESULTS: A decrease in both absolute mast cell numbers staining with mast cell tryptase (AA1) and the percentage of mast cells co-immunostaining with 5-lipoxygenase was seen in the ASA patients after lysine aspirin challenge compared with the non-ASA control group. Aspirin 181-184 arachidonate 5-lipoxygenase Homo sapiens 150-164 8658372-7 1996 RESULTS: A decrease in both absolute mast cell numbers staining with mast cell tryptase (AA1) and the percentage of mast cells co-immunostaining with 5-lipoxygenase was seen in the ASA patients after lysine aspirin challenge compared with the non-ASA control group. Aspirin 247-250 arachidonate 5-lipoxygenase Homo sapiens 150-164 8256883-0 1993 The pivotal role of 5-lipoxygenase products in the reaction of aspirin-sensitive asthmatics to aspirin. Aspirin 63-70 arachidonate 5-lipoxygenase Homo sapiens 20-34 7798537-16 1994 This mediator profile is consistent with mast cell activation during the nasal response to aspirin and suggests that 5-lipoxygenase products are essential for the nasal response to aspirin. Aspirin 181-188 arachidonate 5-lipoxygenase Homo sapiens 117-131 8091318-0 1994 Effect of the 5-lipoxygenase inhibitor ZD2138 on aspirin-induced asthma. Aspirin 49-56 arachidonate 5-lipoxygenase Homo sapiens 14-28 8091318-3 1994 If the cysteinyl leukotrienes cause aspirin-induced asthmatic reactions, inhibition of the 5-lipoxygenase pathway should prevent aspirin-induced bronchospasm. Aspirin 129-136 arachidonate 5-lipoxygenase Homo sapiens 91-105 8091318-11 1994 CONCLUSIONS: In aspirin-sensitive asthma the 5-lipoxygenase inhibitor ZD2138 inhibits the fall in FEV1 induced by aspirin and this is associated with substantial inhibition of 5-lipoxygenase. Aspirin 16-23 arachidonate 5-lipoxygenase Homo sapiens 45-59 8091318-11 1994 CONCLUSIONS: In aspirin-sensitive asthma the 5-lipoxygenase inhibitor ZD2138 inhibits the fall in FEV1 induced by aspirin and this is associated with substantial inhibition of 5-lipoxygenase. Aspirin 114-121 arachidonate 5-lipoxygenase Homo sapiens 45-59 8256883-0 1993 The pivotal role of 5-lipoxygenase products in the reaction of aspirin-sensitive asthmatics to aspirin. Aspirin 95-102 arachidonate 5-lipoxygenase Homo sapiens 20-34 2845746-5 1988 The different effects of NSAIDs on 5-lipoxygenase activity may be of importance in their therapeutic actions as well as in the appearance of some side-effects, e.g. gastric irritation and "aspirin-induced" asthma. Aspirin 189-196 arachidonate 5-lipoxygenase Homo sapiens 35-49 1309376-1 1992 The etiology of aspirin-sensitive asthma is unknown, but a plausible hypothesis is that the inhibitory effect of aspirin on the cyclooxygenase enzyme increases formation of bronchoconstrictor leukotrienes via "shunting" of unmetabolized arachidonic acid into metabolism by the 5-lipoxygenase enzyme. Aspirin 113-120 arachidonate 5-lipoxygenase Homo sapiens 277-291 1651667-9 1991 Acetylsalicylic acid increased 5-lipoxygenase product formation in the coculture studies but not in the isolated cell experiments. Aspirin 0-20 arachidonate 5-lipoxygenase Homo sapiens 31-45 6432882-4 1984 Concentrations of drugs required for 50% inhibition of 5-lipoxygenase were 0.17mM for indomethacin, 0.60mM for ibuprofen, and 3.4mM for aspirin. Aspirin 136-143 arachidonate 5-lipoxygenase Homo sapiens 55-69