PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 27834148-4 2017 A growing body of evidence supports the notion that PPARalpha is activated by natural ligands such as the anorexic lipid mediator oleoylethanolamide (OEA) or synthetic compounds including Wy14643 whereas antagonists like MK-886 block the neurobiological outcomes of PPARalpha. MK-886 221-227 peroxisome proliferator activated receptor alpha Homo sapiens 52-61 27834148-4 2017 A growing body of evidence supports the notion that PPARalpha is activated by natural ligands such as the anorexic lipid mediator oleoylethanolamide (OEA) or synthetic compounds including Wy14643 whereas antagonists like MK-886 block the neurobiological outcomes of PPARalpha. MK-886 221-227 peroxisome proliferator activated receptor alpha Homo sapiens 266-275 27496805-9 2016 These renoprotective effects of Irbe were reversed by the PPARalpha antagonist MK886 and were not detected in Irbe-treated-PON-KO mice. MK-886 79-84 peroxisome proliferator activated receptor alpha Mus musculus 58-67 27477678-8 2016 MK-886, a well-known 5-LOX activating protein (FLAP) inhibitor that also acts on LTC4S, consistently inhibited LTC4 formation in all assay types (IC50=3.1-3.5muM) and we successfully confirmed TK04a as potent LTC4S inhibitor in these assay systems (IC50=17 and 300nM, respectively). MK-886 0-6 leukotriene C4 synthase Homo sapiens 81-86 27477678-8 2016 MK-886, a well-known 5-LOX activating protein (FLAP) inhibitor that also acts on LTC4S, consistently inhibited LTC4 formation in all assay types (IC50=3.1-3.5muM) and we successfully confirmed TK04a as potent LTC4S inhibitor in these assay systems (IC50=17 and 300nM, respectively). MK-886 0-6 leukotriene C4 synthase Homo sapiens 209-214 27495989-11 2016 Adiponectin treatment increased IGFBP-1 levels in primary cultured human trophoblast cells, while the PPARalpha antagonist, MK886, abolished this stimulatory effect. MK-886 124-129 peroxisome proliferator activated receptor alpha Homo sapiens 102-111 27958735-4 2016 Furthermore, 1 induced the expression of PPARalpha-regulated genes involved in lipid, glucose, and cholesterol metabolism, such as CPT-1, PPARalpha, PDK4, and ABCA1, which was abrogated by the PPARalpha antagonist MK-886, indicating that the effect of 1 was dependent on PPARalpha activation. MK-886 214-220 peroxisome proliferator activated receptor alpha Homo sapiens 41-50 27958735-4 2016 Furthermore, 1 induced the expression of PPARalpha-regulated genes involved in lipid, glucose, and cholesterol metabolism, such as CPT-1, PPARalpha, PDK4, and ABCA1, which was abrogated by the PPARalpha antagonist MK-886, indicating that the effect of 1 was dependent on PPARalpha activation. MK-886 214-220 carnitine palmitoyltransferase 1A Homo sapiens 131-136 27958735-4 2016 Furthermore, 1 induced the expression of PPARalpha-regulated genes involved in lipid, glucose, and cholesterol metabolism, such as CPT-1, PPARalpha, PDK4, and ABCA1, which was abrogated by the PPARalpha antagonist MK-886, indicating that the effect of 1 was dependent on PPARalpha activation. MK-886 214-220 peroxisome proliferator activated receptor alpha Homo sapiens 138-147 27958735-4 2016 Furthermore, 1 induced the expression of PPARalpha-regulated genes involved in lipid, glucose, and cholesterol metabolism, such as CPT-1, PPARalpha, PDK4, and ABCA1, which was abrogated by the PPARalpha antagonist MK-886, indicating that the effect of 1 was dependent on PPARalpha activation. MK-886 214-220 pyruvate dehydrogenase kinase 4 Homo sapiens 149-153 27958735-4 2016 Furthermore, 1 induced the expression of PPARalpha-regulated genes involved in lipid, glucose, and cholesterol metabolism, such as CPT-1, PPARalpha, PDK4, and ABCA1, which was abrogated by the PPARalpha antagonist MK-886, indicating that the effect of 1 was dependent on PPARalpha activation. MK-886 214-220 ATP binding cassette subfamily A member 1 Homo sapiens 159-164 27958735-4 2016 Furthermore, 1 induced the expression of PPARalpha-regulated genes involved in lipid, glucose, and cholesterol metabolism, such as CPT-1, PPARalpha, PDK4, and ABCA1, which was abrogated by the PPARalpha antagonist MK-886, indicating that the effect of 1 was dependent on PPARalpha activation. MK-886 214-220 peroxisome proliferator activated receptor alpha Homo sapiens 138-147 27958735-4 2016 Furthermore, 1 induced the expression of PPARalpha-regulated genes involved in lipid, glucose, and cholesterol metabolism, such as CPT-1, PPARalpha, PDK4, and ABCA1, which was abrogated by the PPARalpha antagonist MK-886, indicating that the effect of 1 was dependent on PPARalpha activation. MK-886 214-220 peroxisome proliferator activated receptor alpha Homo sapiens 138-147 26754842-0 2016 MK886 inhibits the pioglitazone-induced anti-invasion of MDA-MB-231 cells is associated with PPARalpha/gamma, FGF4 and 5LOX. MK-886 0-5 peroxisome proliferator activated receptor alpha Homo sapiens 93-102 26754842-0 2016 MK886 inhibits the pioglitazone-induced anti-invasion of MDA-MB-231 cells is associated with PPARalpha/gamma, FGF4 and 5LOX. MK-886 0-5 fibroblast growth factor 4 Homo sapiens 110-114 26754842-1 2016 The goal of this study was to determine the effects of PGZ and MK886 on the mRNA expression of PPARalpha and other associated genes in MDA-MB-231 cells, and the biological mechanisms induced by both drugs were also assessed. MK-886 63-68 peroxisome proliferator activated receptor alpha Homo sapiens 95-104 26754842-2 2016 The levels of PPARalpha mRNA expression in PGZ-treated and MK886-treated MDA-MB-231 cells were determined using real-time PCR; the growth inhibitory effects of PGZ and MK886 were determined using the trypan blue exclusion assay; the induction of apoptosis by PGZ and MK886 was determined using DNA fragmentation assay and real-time PCR; and the invasion of PGZ-treated and MK886-treated MDA-MB-231 cells was determined using the wound healing and transwell migration assays. MK-886 59-64 peroxisome proliferator activated receptor alpha Homo sapiens 14-23 26754842-4 2016 Our results demonstrated that the treatment of MDA-MB-231 cells with PGZ increased the expression of PPARalpha/gamma mRNA and that this expression could be inhibited by treatment with MK886. MK-886 184-189 peroxisome proliferator activated receptor alpha Homo sapiens 101-110 27100490-5 2016 The mRNA and protein levels of CPT-Ialpha gene from HepG2 cells and hyperlipidemic rat liver are remarkably up-regulated by berberine, and this effect can be blocked by MK886, a non-competitive antagonist of PPARalpha. MK-886 169-174 peroxisome proliferator activated receptor alpha Rattus norvegicus 208-217 27646482-9 2016 However, similar findings from the sham of vehicle groups were observed if PPARalpha antagonist MK-886 was administered to rats (10, 20, 30mg/Kg, i.p.). MK-886 96-102 peroxisome proliferator activated receptor alpha Rattus norvegicus 75-84 26072684-6 2015 Peak responses were significantly reduced by administration of the glucocorticoid dexamethasone, the H1 receptor antagonist diphenhydramine and the FLAP inhibitor MK-886. MK-886 163-169 arachidonate 5-lipoxygenase activating protein Rattus norvegicus 148-152 27229177-7 2016 We further investigated the effect of NAMPT knockdown on the PPARalpha-LXRalpha pathway of cholesterol metabolism with MK886 (a selective inhibitor of PPARalpha) in RAW264.7 macrophages. MK-886 119-124 nicotinamide phosphoribosyltransferase Mus musculus 38-43 27229177-7 2016 We further investigated the effect of NAMPT knockdown on the PPARalpha-LXRalpha pathway of cholesterol metabolism with MK886 (a selective inhibitor of PPARalpha) in RAW264.7 macrophages. MK-886 119-124 peroxisome proliferator activated receptor alpha Mus musculus 61-70 27229177-7 2016 We further investigated the effect of NAMPT knockdown on the PPARalpha-LXRalpha pathway of cholesterol metabolism with MK886 (a selective inhibitor of PPARalpha) in RAW264.7 macrophages. MK-886 119-124 nuclear receptor subfamily 1, group H, member 3 Mus musculus 71-79 27229177-8 2016 MK886 abolished the ability of NAMPT knockdown to decrease intracellular cholesterol levels to enhance the rate of (3)H-cholesterol efflux and to increase ABCA1/G1 and LXRalpha expressions in RAW264.7 macrophages. MK-886 0-5 nicotinamide phosphoribosyltransferase Mus musculus 31-36 27229177-8 2016 MK886 abolished the ability of NAMPT knockdown to decrease intracellular cholesterol levels to enhance the rate of (3)H-cholesterol efflux and to increase ABCA1/G1 and LXRalpha expressions in RAW264.7 macrophages. MK-886 0-5 ATP-binding cassette, sub-family A (ABC1), member 1 Mus musculus 155-160 27229177-8 2016 MK886 abolished the ability of NAMPT knockdown to decrease intracellular cholesterol levels to enhance the rate of (3)H-cholesterol efflux and to increase ABCA1/G1 and LXRalpha expressions in RAW264.7 macrophages. MK-886 0-5 nuclear receptor subfamily 1, group H, member 3 Mus musculus 168-176 26040494-8 2015 The effects of these 15-LOX inhibitors were maintained in the presence of indomethacin and MK886. MK-886 91-96 arachidonate 15-lipoxygenase Homo sapiens 21-27 25304895-5 2014 Luciferase assay showed that 12 increased the transcriptional activity of PPARalpha, while its lipid-lowering effect was abolished by PPARalpha inhibitor, MK886, in HepG2 cells. MK-886 155-160 peroxisome proliferator activated receptor alpha Homo sapiens 134-143 25754762-4 2015 The effects of FAAH inhibition on nicotine self-administration and nicotine priming-induced reinstatement were reversed by the PPAR-alpha antagonist, MK886. MK-886 150-155 fatty acid amide hydrolase Homo sapiens 15-19 25754762-4 2015 The effects of FAAH inhibition on nicotine self-administration and nicotine priming-induced reinstatement were reversed by the PPAR-alpha antagonist, MK886. MK-886 150-155 peroxisome proliferator activated receptor alpha Homo sapiens 127-137 26003114-10 2015 Although BCRP downregulation was not confirmed as leading mechanism responsible for elevated levels of hypericin content, changes in expression and efflux activity of ABC transporters caused by MK-886 suggest its potential in combination treatment with drugs that are substrates of these transporters, predominantly MRP1. MK-886 194-200 ATP binding cassette subfamily C member 1 Homo sapiens 316-320 26310614-9 2015 on various animal models were abolished in PPAR-alpha(-/-) mice, and were prevented by PPAR-alpha antagonist MK886 but not by canabinoid receptor type 1 (CB1) antagonist Rimonabant nor canabinoid receptor type 2 (CB2) antagonist SR144528. MK-886 109-114 peroxisome proliferator activated receptor alpha Mus musculus 43-53 26310614-9 2015 on various animal models were abolished in PPAR-alpha(-/-) mice, and were prevented by PPAR-alpha antagonist MK886 but not by canabinoid receptor type 1 (CB1) antagonist Rimonabant nor canabinoid receptor type 2 (CB2) antagonist SR144528. MK-886 109-114 peroxisome proliferator activated receptor alpha Mus musculus 87-97 26310614-9 2015 on various animal models were abolished in PPAR-alpha(-/-) mice, and were prevented by PPAR-alpha antagonist MK886 but not by canabinoid receptor type 1 (CB1) antagonist Rimonabant nor canabinoid receptor type 2 (CB2) antagonist SR144528. MK-886 109-114 cannabinoid receptor 2 (macrophage) Mus musculus 213-216 25729765-9 2015 Administration of MK886 before perfusion with NaT also significantly reduced the severity of pancreatitis in wild-type mice. MK-886 18-23 solute carrier family 38, member 3 Mus musculus 46-49 24905297-8 2014 Only in cells expressing FLAP and 5-LO, the FLAP antagonist MK886 blocked FLAP-mediated increase in 5-LO product formation, and prevented 5-LO nuclear membrane translocation and co-localization with FLAP. MK-886 60-65 arachidonate 5-lipoxygenase activating protein Homo sapiens 25-29 24905297-8 2014 Only in cells expressing FLAP and 5-LO, the FLAP antagonist MK886 blocked FLAP-mediated increase in 5-LO product formation, and prevented 5-LO nuclear membrane translocation and co-localization with FLAP. MK-886 60-65 arachidonate 5-lipoxygenase activating protein Homo sapiens 44-48 24905297-8 2014 Only in cells expressing FLAP and 5-LO, the FLAP antagonist MK886 blocked FLAP-mediated increase in 5-LO product formation, and prevented 5-LO nuclear membrane translocation and co-localization with FLAP. MK-886 60-65 arachidonate 5-lipoxygenase activating protein Homo sapiens 44-48 24905297-8 2014 Only in cells expressing FLAP and 5-LO, the FLAP antagonist MK886 blocked FLAP-mediated increase in 5-LO product formation, and prevented 5-LO nuclear membrane translocation and co-localization with FLAP. MK-886 60-65 arachidonate 5-lipoxygenase activating protein Homo sapiens 44-48 24067162-8 2014 Similarly, 1 micromol/L and 10 mumol/L telmisartan significantly increased the expression of LPL mRNA and protein in HepG2 cells (p < 0.01), and this increase was significantly (p < 0.01) inhibited by the PPAR-alpha-specific antagonist MK886. MK-886 242-247 lipoprotein lipase Homo sapiens 93-96 24743022-1 2014 We have previously described that arachidonic acid (AA)-5-lipoxygenase (5-LO) metabolism inhibitors such as NDGA and MK886, inhibit cell death by apoptosis, but not by necrosis, induced by extracellular ATP (ATPe) binding to P2X7 receptors in macrophages. MK-886 117-122 arachidonate 5-lipoxygenase Mus musculus 56-70 24743022-1 2014 We have previously described that arachidonic acid (AA)-5-lipoxygenase (5-LO) metabolism inhibitors such as NDGA and MK886, inhibit cell death by apoptosis, but not by necrosis, induced by extracellular ATP (ATPe) binding to P2X7 receptors in macrophages. MK-886 117-122 ATP synthase, H+ transporting, mitochondrial F1 complex, epsilon subunit Mus musculus 208-212 24743022-1 2014 We have previously described that arachidonic acid (AA)-5-lipoxygenase (5-LO) metabolism inhibitors such as NDGA and MK886, inhibit cell death by apoptosis, but not by necrosis, induced by extracellular ATP (ATPe) binding to P2X7 receptors in macrophages. MK-886 117-122 purinergic receptor P2X, ligand-gated ion channel, 7 Mus musculus 225-229 25116953-5 2014 In monocytes treated with MK886, a 5-lipoxygenase (LO) inhibitor, both Mac-1 expression and monocyte adhesion to endothelial cells induced by KLA were markedly attenuated. MK-886 26-31 arachidonate 5-lipoxygenase Mus musculus 35-49 25116953-5 2014 In monocytes treated with MK886, a 5-lipoxygenase (LO) inhibitor, both Mac-1 expression and monocyte adhesion to endothelial cells induced by KLA were markedly attenuated. MK-886 26-31 integrin alpha M Mus musculus 71-76 24681156-4 2014 Here, we investigate the efficacy of MK-886, an inhibitor of 5-lipoxygenase activating protein (FLAP), in blocking leukotriene synthesis, secondary brain damage, synaptic dysfunction, and cognitive impairments after TBI. MK-886 37-43 arachidonate 5-lipoxygenase activating protein Homo sapiens 96-100 24681156-8 2014 MK-886 significantly attenuated blood-brain barrier disruption in the CA1 hippocampal region and deficits in long-term potentiation (LTP) at CA1 hippocampal synapses. MK-886 0-6 carbonic anhydrase 1 Homo sapiens 70-73 24681156-8 2014 MK-886 significantly attenuated blood-brain barrier disruption in the CA1 hippocampal region and deficits in long-term potentiation (LTP) at CA1 hippocampal synapses. MK-886 0-6 carbonic anhydrase 1 Homo sapiens 141-144 24274060-6 2014 Herein we report the discovery of the first small molecule VopS inhibitors (e.g., calmidazolium, GW7647, and MK886) with Ki"s ranging from 6 to 50 muM and upward of 30-fold selectivity versus HYPE, the only known human AMPylator. MK-886 109-114 FIC domain protein adenylyltransferase Homo sapiens 192-196 24021653-5 2014 RESULTS: We found that MK886 significantly reduced brain levels of nicastrin and PPARalpha, but did not affect levels of beta-secretase, apolipoprotein E or low-density lipoprotein receptor-related protein-1. MK-886 23-28 peroxisome proliferator activated receptor alpha Mus musculus 81-90 24068329-10 2014 H2O2 and MK886 both reduced the viability of HepG2 cells, increased oxidative stress and apoptosis, up-regulated the BiP and CHOP expression, and induced CHOP translocation from the cytoplasm to the nucleus. MK-886 9-14 heat shock protein family A (Hsp70) member 5 Homo sapiens 117-120 24068329-10 2014 H2O2 and MK886 both reduced the viability of HepG2 cells, increased oxidative stress and apoptosis, up-regulated the BiP and CHOP expression, and induced CHOP translocation from the cytoplasm to the nucleus. MK-886 9-14 DNA damage inducible transcript 3 Homo sapiens 125-129 24068329-10 2014 H2O2 and MK886 both reduced the viability of HepG2 cells, increased oxidative stress and apoptosis, up-regulated the BiP and CHOP expression, and induced CHOP translocation from the cytoplasm to the nucleus. MK-886 9-14 DNA damage inducible transcript 3 Homo sapiens 154-158 24693335-4 2014 Leukotriene receptor antagonist MK571 and 5-lipoxygenase inhibitor MK886 were used for pharmacologic intervention. MK-886 67-72 arachidonate 5-lipoxygenase Rattus norvegicus 42-56 24168271-8 2013 Production of leukotriene B4 was associated with an increase in 5-lipoxygenase expression in human neutrophils; addition of MK886 (a 5-lipoxygenase activating protein inhibitor) attenuated further increase in leukotriene B4 production. MK-886 124-129 arachidonate 5-lipoxygenase Homo sapiens 133-147 23978332-8 2013 The PPARalpha antagonist MK886 restored the beta-catenin and E-cadherin expression levels in Jeg-3 cells and reversed the suppression of the spheroid attachment caused by PFOA. MK-886 25-30 peroxisome proliferator activated receptor alpha Homo sapiens 4-13 23978332-8 2013 The PPARalpha antagonist MK886 restored the beta-catenin and E-cadherin expression levels in Jeg-3 cells and reversed the suppression of the spheroid attachment caused by PFOA. MK-886 25-30 catenin beta 1 Homo sapiens 44-56 23978332-8 2013 The PPARalpha antagonist MK886 restored the beta-catenin and E-cadherin expression levels in Jeg-3 cells and reversed the suppression of the spheroid attachment caused by PFOA. MK-886 25-30 cadherin 1 Homo sapiens 61-71 23998390-11 2013 These effects were inhibited by the PPAR-alpha antagonist MK886. MK-886 58-63 peroxisome proliferator activated receptor alpha Homo sapiens 36-46 23800665-6 2013 MK-886, a specific inhibitor of 5-LOX activating protein (FLAP), significantly increased [(3)H]-dopamine uptake, a functional indicator of the integrity of dopaminergic neurons, in midbrain cultures or the SH-SY5Y human dopaminergic cell line following MPP(+) treatment. MK-886 0-6 lysyl oxidase Mus musculus 34-37 24167735-9 2013 Both MK-886 and DITPA significantly counteract the increase in the levels of cardiac TNF- alpha , IL-1 beta , and ICAM-1 and plasma level of cTnI (P < 0.05). MK-886 5-11 tumor necrosis factor Rattus norvegicus 85-95 24167735-9 2013 Both MK-886 and DITPA significantly counteract the increase in the levels of cardiac TNF- alpha , IL-1 beta , and ICAM-1 and plasma level of cTnI (P < 0.05). MK-886 5-11 interleukin 1 beta Rattus norvegicus 98-107 24167735-9 2013 Both MK-886 and DITPA significantly counteract the increase in the levels of cardiac TNF- alpha , IL-1 beta , and ICAM-1 and plasma level of cTnI (P < 0.05). MK-886 5-11 intercellular adhesion molecule 1 Rattus norvegicus 114-120 23889688-5 2013 These effects were abolished in the presence of the PPAR-alpha antagonist MK886. MK-886 74-79 peroxisome proliferator activated receptor alpha Rattus norvegicus 52-62 23305233-7 2013 MK886 was found to inhibit the activity of all DNA polymerases tested with similar IC(50) values, the exception being a 6- to 8-fold increase in the potency of inhibition against human DNA polymerase iota (hpol iota), a highly error-prone enzyme that uses Hoogsteen base-pairing modes during catalysis. MK-886 0-5 DNA polymerase iota Homo sapiens 185-204 23160450-7 2013 The PPARalpha antagonist MK886 killed circulating CLL cells directly, caused proliferating CLL cells to enter an immunogenic death pathway and cleared CLL xenografts from immunodeficient mice. MK-886 25-30 peroxisome proliferator activated receptor alpha Mus musculus 4-13 23844263-4 2013 The effects of PGI2 were abrogated by MK886, a PPARalpha antagonist, but not GSK3787, a PPARdelta antagonist. MK-886 38-43 peroxisome proliferator activated receptor alpha Rattus norvegicus 47-56 23724059-12 2013 Acute WY effects were reverted by the PPARalpha antagonist MK886 (3 mg/kg, i.p.). MK-886 59-64 peroxisome proliferator activated receptor alpha Mus musculus 38-47 23238934-6 2013 Ablation of L-FABP or PPARalpha as well as treatment with MK886 (PPARalpha inhibitor) abolished/reduced PUFA-mediated PPARalpha transcription of these genes, especially at high glucose. MK-886 58-63 peroxisome proliferator activated receptor alpha Mus musculus 65-74 23261452-0 2013 Lipoxygenase inhibitor MK886 potentiates TRAIL-induced apoptosis through CHOP- and p38 MAPK-mediated up-regulation of death receptor 5 in malignant glioma. MK-886 23-28 TNF superfamily member 10 Homo sapiens 41-46 23261452-0 2013 Lipoxygenase inhibitor MK886 potentiates TRAIL-induced apoptosis through CHOP- and p38 MAPK-mediated up-regulation of death receptor 5 in malignant glioma. MK-886 23-28 DNA damage inducible transcript 3 Homo sapiens 73-77 23261452-0 2013 Lipoxygenase inhibitor MK886 potentiates TRAIL-induced apoptosis through CHOP- and p38 MAPK-mediated up-regulation of death receptor 5 in malignant glioma. MK-886 23-28 mitogen-activated protein kinase 14 Homo sapiens 83-86 23261452-0 2013 Lipoxygenase inhibitor MK886 potentiates TRAIL-induced apoptosis through CHOP- and p38 MAPK-mediated up-regulation of death receptor 5 in malignant glioma. MK-886 23-28 TNF receptor superfamily member 10b Homo sapiens 118-134 23261452-4 2013 In this study, we elucidated the molecular mechanisms responsible for MK886-mediated sensitization to TRAIL-induced apoptosis. MK-886 70-75 TNF superfamily member 10 Homo sapiens 102-107 23261452-5 2013 We found that MK886 sensitized glioma cells to TRAIL-induced apoptosis by upregulating the death receptor 5 (DR5) and that specific knockdown of DR5 attenuated cell death. MK-886 14-19 TNF superfamily member 10 Homo sapiens 47-52 23261452-5 2013 We found that MK886 sensitized glioma cells to TRAIL-induced apoptosis by upregulating the death receptor 5 (DR5) and that specific knockdown of DR5 attenuated cell death. MK-886 14-19 TNF receptor superfamily member 10b Homo sapiens 91-107 23261452-5 2013 We found that MK886 sensitized glioma cells to TRAIL-induced apoptosis by upregulating the death receptor 5 (DR5) and that specific knockdown of DR5 attenuated cell death. MK-886 14-19 TNF receptor superfamily member 10b Homo sapiens 109-112 23261452-6 2013 The mechanisms underlying this sensitization involved activation of the MK886-induced p38 mitogen-activated protein kinase (MAPK) pathway and subsequent DR5 overexpression. MK-886 72-77 mitogen-activated protein kinase 14 Homo sapiens 86-89 23261452-6 2013 The mechanisms underlying this sensitization involved activation of the MK886-induced p38 mitogen-activated protein kinase (MAPK) pathway and subsequent DR5 overexpression. MK-886 72-77 TNF receptor superfamily member 10b Homo sapiens 153-156 23261452-8 2013 Taken together, our findings indicate that the increased expression of DR5 in a p38 MAPK-dependent manner plays an important role in the sensitization of MK886 to TRAIL-induced apoptosis. MK-886 154-159 TNF receptor superfamily member 10b Homo sapiens 71-74 23261452-8 2013 Taken together, our findings indicate that the increased expression of DR5 in a p38 MAPK-dependent manner plays an important role in the sensitization of MK886 to TRAIL-induced apoptosis. MK-886 154-159 mitogen-activated protein kinase 14 Homo sapiens 80-83 23261452-8 2013 Taken together, our findings indicate that the increased expression of DR5 in a p38 MAPK-dependent manner plays an important role in the sensitization of MK886 to TRAIL-induced apoptosis. MK-886 154-159 TNF superfamily member 10 Homo sapiens 163-168 23238934-6 2013 Ablation of L-FABP or PPARalpha as well as treatment with MK886 (PPARalpha inhibitor) abolished/reduced PUFA-mediated PPARalpha transcription of these genes, especially at high glucose. MK-886 58-63 peroxisome proliferator activated receptor alpha Mus musculus 65-74 23573121-9 2013 MK886 (0.3 mu mol/L), a selective PPAR alpha antagonist, could abolish the effects of berberine and fenofibrate. MK-886 0-5 peroxisome proliferator activated receptor alpha Rattus norvegicus 35-45 23762565-2 2013 Cells were treated with olanzapine and a 5-lipoxygenase (5-LOX) activating protein (FLAP) inhibitor MK-886. MK-886 100-106 arachidonate 5-lipoxygenase Homo sapiens 41-55 23762565-2 2013 Cells were treated with olanzapine and a 5-lipoxygenase (5-LOX) activating protein (FLAP) inhibitor MK-886. MK-886 100-106 arachidonate 5-lipoxygenase Homo sapiens 57-62 23762565-2 2013 Cells were treated with olanzapine and a 5-lipoxygenase (5-LOX) activating protein (FLAP) inhibitor MK-886. MK-886 100-106 arachidonate 5-lipoxygenase activating protein Homo sapiens 84-88 23129255-7 2013 The involvement of PPARalpha was demonstrated by treatment with the antagonist MK-886. MK-886 79-85 peroxisome proliferator activated receptor alpha Mus musculus 19-28 23187752-6 2013 The PAF hyperalgesic mechanisms were dependent on prostaglandins, leukotrienes and neutrophils, as PAF-induced articular hyperalgesia was inhibited by indomethacin (COX inhibitor), MK886 (leukotrienes synthesis inhibitor) or fucoidan (leukocyte rolling inhibitor). MK-886 181-186 patchy fur Mus musculus 4-7 23187752-6 2013 The PAF hyperalgesic mechanisms were dependent on prostaglandins, leukotrienes and neutrophils, as PAF-induced articular hyperalgesia was inhibited by indomethacin (COX inhibitor), MK886 (leukotrienes synthesis inhibitor) or fucoidan (leukocyte rolling inhibitor). MK-886 181-186 patchy fur Mus musculus 99-102 23022336-4 2012 Both MK886 [(1-[(4-chlorophenyl)methyl]-3-1,1-dimethylethyl)thio]-(alpha,alpha-dimethyl-5-1-methylethyl)-1H-indole-2-propanoic acid (PPARalpha antagonist) and GW9662 (2-chloro-5-nitrobenzanilide) (PPARgamma antagonists) inhibited Wy14643-induced relaxations. MK-886 5-10 peroxisome proliferator activated receptor alpha Rattus norvegicus 133-142 23022336-4 2012 Both MK886 [(1-[(4-chlorophenyl)methyl]-3-1,1-dimethylethyl)thio]-(alpha,alpha-dimethyl-5-1-methylethyl)-1H-indole-2-propanoic acid (PPARalpha antagonist) and GW9662 (2-chloro-5-nitrobenzanilide) (PPARgamma antagonists) inhibited Wy14643-induced relaxations. MK-886 5-10 peroxisome proliferator-activated receptor gamma Rattus norvegicus 197-206 23114121-1 2012 To investigate the effect of a microsomal prostaglandin E synthase-1 (mPGES-1) inhibitor MK886 on cell cycle of the human acute myeloid leukemia HL-60 cells. MK-886 89-94 prostaglandin E synthase Mus musculus 70-77 23114121-0 2012 [Effect of mPGES-1 inhibitor MK886 on cell cycle of leukemia HL-60 cells]. MK-886 29-34 prostaglandin E synthase Mus musculus 11-18 23114121-3 2012 The results indicated that after treated with MK886, the percentage of HL-60 cells decreased in G(0)/G(1) phase and increased in S phase, and expressions of mPGES-1, cyclin D1, P-Akt and C-MYC and synthesis of PGE(2) decreased significantly. MK-886 46-51 prostaglandin E synthase Mus musculus 157-164 23114121-1 2012 To investigate the effect of a microsomal prostaglandin E synthase-1 (mPGES-1) inhibitor MK886 on cell cycle of the human acute myeloid leukemia HL-60 cells. MK-886 89-94 prostaglandin E synthase Homo sapiens 31-68 23114121-3 2012 The results indicated that after treated with MK886, the percentage of HL-60 cells decreased in G(0)/G(1) phase and increased in S phase, and expressions of mPGES-1, cyclin D1, P-Akt and C-MYC and synthesis of PGE(2) decreased significantly. MK-886 46-51 cyclin D1 Homo sapiens 166-175 23114121-3 2012 The results indicated that after treated with MK886, the percentage of HL-60 cells decreased in G(0)/G(1) phase and increased in S phase, and expressions of mPGES-1, cyclin D1, P-Akt and C-MYC and synthesis of PGE(2) decreased significantly. MK-886 46-51 AKT serine/threonine kinase 1 Homo sapiens 179-182 23114121-3 2012 The results indicated that after treated with MK886, the percentage of HL-60 cells decreased in G(0)/G(1) phase and increased in S phase, and expressions of mPGES-1, cyclin D1, P-Akt and C-MYC and synthesis of PGE(2) decreased significantly. MK-886 46-51 MYC proto-oncogene, bHLH transcription factor Homo sapiens 187-192 23114121-4 2012 It is concluded that MK886 can arrest HL-60 cells in G(0)/G(1) phase, the mechanism of which is possibly associated to inhibition of mPGES-1 expression, reduction of PGE(2) synthesis, suppression of Akt phosphorylation and C-MYC expression, down-regulation of cyclin D1 expression. MK-886 21-26 prostaglandin E synthase Mus musculus 133-140 23114121-4 2012 It is concluded that MK886 can arrest HL-60 cells in G(0)/G(1) phase, the mechanism of which is possibly associated to inhibition of mPGES-1 expression, reduction of PGE(2) synthesis, suppression of Akt phosphorylation and C-MYC expression, down-regulation of cyclin D1 expression. MK-886 21-26 AKT serine/threonine kinase 1 Homo sapiens 199-202 23114121-4 2012 It is concluded that MK886 can arrest HL-60 cells in G(0)/G(1) phase, the mechanism of which is possibly associated to inhibition of mPGES-1 expression, reduction of PGE(2) synthesis, suppression of Akt phosphorylation and C-MYC expression, down-regulation of cyclin D1 expression. MK-886 21-26 MYC proto-oncogene, bHLH transcription factor Homo sapiens 223-228 23114121-4 2012 It is concluded that MK886 can arrest HL-60 cells in G(0)/G(1) phase, the mechanism of which is possibly associated to inhibition of mPGES-1 expression, reduction of PGE(2) synthesis, suppression of Akt phosphorylation and C-MYC expression, down-regulation of cyclin D1 expression. MK-886 21-26 cyclin D1 Homo sapiens 260-269 22931637-0 2012 [Effect of mPGES-1 inhibitor MK886 on apoptosis and drug resistance of HL-60/A cells]. MK-886 29-34 prostaglandin E synthase Mus musculus 11-18 22962275-2 2012 Here, we show that therapeutic combination of the lipoxygenase inhibitor MK886 and TRAIL-secreting human mesenchymal stem cells (MSC-TRAIL) provide targeted and prolonged delivery of TRAIL both in vitro and in orthotopic mouse models of glioma. MK-886 73-78 TNF superfamily member 10 Homo sapiens 133-138 22962275-2 2012 Here, we show that therapeutic combination of the lipoxygenase inhibitor MK886 and TRAIL-secreting human mesenchymal stem cells (MSC-TRAIL) provide targeted and prolonged delivery of TRAIL both in vitro and in orthotopic mouse models of glioma. MK-886 73-78 TNF superfamily member 10 Homo sapiens 133-138 22962275-4 2012 MK886 effectively increased the sensitivity to TRAIL-induced apoptosis via upregulation of the death receptor 5 and downregulation of the antiapoptotic protein survivin in human glioma cell lines and in primary glioma cells. MK-886 0-5 TNF superfamily member 10 Homo sapiens 47-52 22962275-4 2012 MK886 effectively increased the sensitivity to TRAIL-induced apoptosis via upregulation of the death receptor 5 and downregulation of the antiapoptotic protein survivin in human glioma cell lines and in primary glioma cells. MK-886 0-5 TNF receptor superfamily member 10b Homo sapiens 95-111 22480617-6 2012 In some experiments, the PPARalpha antagonist MK886 (10mg/kg, ig) was administered 0.5h before OEA. MK-886 46-51 peroxisome proliferator activated receptor alpha Mus musculus 25-34 22480617-13 2012 The PPARalpha antagonist MK886 abolished the protective effects of OEA. MK-886 25-30 peroxisome proliferator activated receptor alpha Mus musculus 4-13 22931637-1 2012 This study was aimed to investigate the effect of MK886, a mPGES-1 inhibitor, on apoptosis and drug resistance of leukemia HL-60/A cell line. MK-886 50-55 prostaglandin E synthase Mus musculus 59-66 22931637-11 2012 It is concluded that MK886 can inhibit HL-60/A cell proliferation, induce apoptosis and enhance sensitivity to chemotherapeutic drugs, the mechanism of which possibly associates to down-regulation of mPGES-1/PGE2 synthesis, reduction P-Akt expression and decreasing mdr-1 and P170 protein expression. MK-886 21-26 prostaglandin E synthase Mus musculus 200-207 22931637-11 2012 It is concluded that MK886 can inhibit HL-60/A cell proliferation, induce apoptosis and enhance sensitivity to chemotherapeutic drugs, the mechanism of which possibly associates to down-regulation of mPGES-1/PGE2 synthesis, reduction P-Akt expression and decreasing mdr-1 and P170 protein expression. MK-886 21-26 AKT serine/threonine kinase 1 Homo sapiens 236-239 22931637-11 2012 It is concluded that MK886 can inhibit HL-60/A cell proliferation, induce apoptosis and enhance sensitivity to chemotherapeutic drugs, the mechanism of which possibly associates to down-regulation of mPGES-1/PGE2 synthesis, reduction P-Akt expression and decreasing mdr-1 and P170 protein expression. MK-886 21-26 ATP binding cassette subfamily B member 1 Homo sapiens 266-271 22535242-8 2012 The half-life of the CPB2 transcript was shortened by treatment with WY14643 as compared with that of the control, and the decreased half-life of mRNA returned to control levels by treatment with a PPARalpha antagonist MK886 or transfection of PPAR A-specific siRNA to WY14643-treated HepG2 cells. MK-886 221-226 carboxypeptidase B2 Homo sapiens 22-26 22535242-8 2012 The half-life of the CPB2 transcript was shortened by treatment with WY14643 as compared with that of the control, and the decreased half-life of mRNA returned to control levels by treatment with a PPARalpha antagonist MK886 or transfection of PPAR A-specific siRNA to WY14643-treated HepG2 cells. MK-886 221-226 peroxisome proliferator activated receptor alpha Homo sapiens 200-209 21791144-7 2012 However, a combination of ICI182780 and MK886 significantly inhibited resveratrol-induced eNOS mRNA expression. MK-886 40-45 nitric oxide synthase 3 Homo sapiens 90-94 22266374-3 2012 We demonstrate that PPARalpha-selective ligands (i.e., clofibrate, GW7647) significantly induce BCRP mRNA and protein expression in a time- and concentration-dependent manner, whereas pharmacological inhibitors (i.e., MK886, GW6471) prevent this induction. MK-886 218-223 peroxisome proliferator activated receptor alpha Homo sapiens 20-29 22435679-14 2012 Besides, we also found that the promotion of SOD and CAT protein expression induced by L-carnitine was blocked by PPAR-alpha inhibitor MK886. MK-886 135-140 catalase Homo sapiens 53-56 22435679-14 2012 Besides, we also found that the promotion of SOD and CAT protein expression induced by L-carnitine was blocked by PPAR-alpha inhibitor MK886. MK-886 135-140 peroxisome proliferator activated receptor alpha Homo sapiens 114-124 22038016-0 2011 MK886 inhibits the proliferation of HL-60 leukemia cells by suppressing the expression of mPGES-1 and reducing prostaglandin E2 synthesis. MK-886 0-5 prostaglandin E synthase Mus musculus 90-97 21946955-8 2012 Moreover, inhibition of PPARalpha activity by its antagonist MK886 did not significantly reverse the anti-inflammatory effects of biochanin A and genistein, indicating that their anti-inflammatory properties were PPARalpha-independent. MK-886 61-66 peroxisome proliferator activated receptor alpha Mus musculus 24-33 23056190-5 2012 Candesartan cilexetil, manoalide, and MK-886 were selected as proof-of-principle compounds and further characterized for their specificity toward pol kappa by primer extension assays using DNAs containing a site-specific acrolein-derived, ring-opened reduced form of gamma-HOPdG. MK-886 38-44 DNA polymerase lambda Homo sapiens 146-155 22038016-6 2011 We conclude that MK886 reduces the viability of leukemia HL-60 cells by reducing mPGES-1 expression and PGE2 synthesis in a dose-dependent manner, which strongly suggests that mPGES-1 inhibitors should be considered as promising candidates for leukemia treatment. MK-886 17-22 prostaglandin E synthase Mus musculus 81-88 22038016-6 2011 We conclude that MK886 reduces the viability of leukemia HL-60 cells by reducing mPGES-1 expression and PGE2 synthesis in a dose-dependent manner, which strongly suggests that mPGES-1 inhibitors should be considered as promising candidates for leukemia treatment. MK-886 17-22 prostaglandin E synthase Mus musculus 176-183 22293202-3 2012 We found that the treatment of MK886 (an inhibitor of 5-LOX) or knockdown of 5-LOX was able to downregulate the expression of NF-kappaB p65 at the mRNA level and decreased the phosphorylation level of inhibitor kappaBalpha (IkappaBalpha) in the cytoplasm of hepatoma HepG2 or H7402 cells, which resulted in the decrease of the level of nuclear NF-kappaB p65. MK-886 31-36 lysyl oxidase Homo sapiens 56-59 22293202-3 2012 We found that the treatment of MK886 (an inhibitor of 5-LOX) or knockdown of 5-LOX was able to downregulate the expression of NF-kappaB p65 at the mRNA level and decreased the phosphorylation level of inhibitor kappaBalpha (IkappaBalpha) in the cytoplasm of hepatoma HepG2 or H7402 cells, which resulted in the decrease of the level of nuclear NF-kappaB p65. MK-886 31-36 arachidonate 5-lipoxygenase Homo sapiens 54-59 22293202-3 2012 We found that the treatment of MK886 (an inhibitor of 5-LOX) or knockdown of 5-LOX was able to downregulate the expression of NF-kappaB p65 at the mRNA level and decreased the phosphorylation level of inhibitor kappaBalpha (IkappaBalpha) in the cytoplasm of hepatoma HepG2 or H7402 cells, which resulted in the decrease of the level of nuclear NF-kappaB p65. MK-886 31-36 nuclear factor kappa B subunit 1 Homo sapiens 126-135 22293202-3 2012 We found that the treatment of MK886 (an inhibitor of 5-LOX) or knockdown of 5-LOX was able to downregulate the expression of NF-kappaB p65 at the mRNA level and decreased the phosphorylation level of inhibitor kappaBalpha (IkappaBalpha) in the cytoplasm of hepatoma HepG2 or H7402 cells, which resulted in the decrease of the level of nuclear NF-kappaB p65. MK-886 31-36 RELA proto-oncogene, NF-kB subunit Homo sapiens 136-139 22293202-3 2012 We found that the treatment of MK886 (an inhibitor of 5-LOX) or knockdown of 5-LOX was able to downregulate the expression of NF-kappaB p65 at the mRNA level and decreased the phosphorylation level of inhibitor kappaBalpha (IkappaBalpha) in the cytoplasm of hepatoma HepG2 or H7402 cells, which resulted in the decrease of the level of nuclear NF-kappaB p65. MK-886 31-36 NFKB inhibitor alpha Homo sapiens 224-236 22293202-3 2012 We found that the treatment of MK886 (an inhibitor of 5-LOX) or knockdown of 5-LOX was able to downregulate the expression of NF-kappaB p65 at the mRNA level and decreased the phosphorylation level of inhibitor kappaBalpha (IkappaBalpha) in the cytoplasm of hepatoma HepG2 or H7402 cells, which resulted in the decrease of the level of nuclear NF-kappaB p65. MK-886 31-36 nuclear factor kappa B subunit 1 Homo sapiens 344-353 22293202-3 2012 We found that the treatment of MK886 (an inhibitor of 5-LOX) or knockdown of 5-LOX was able to downregulate the expression of NF-kappaB p65 at the mRNA level and decreased the phosphorylation level of inhibitor kappaBalpha (IkappaBalpha) in the cytoplasm of hepatoma HepG2 or H7402 cells, which resulted in the decrease of the level of nuclear NF-kappaB p65. MK-886 31-36 RELA proto-oncogene, NF-kB subunit Homo sapiens 354-357 22068350-6 2012 Similar reduction was achieved by MK-886, an inhibitor of 5-LOX activating protein but the above differences were not statistically significant. MK-886 34-40 arachidonate 5-lipoxygenase Homo sapiens 60-63 22038016-4 2011 Cytotoxicity assays and flow cytometry showed that MK886, an inhibitor of mPGES-1, inhibits proliferation of HL-60 cells and induces apoptosis in a dose- and time-dependent manner, which may result from down-regulation of mPGES-1 expression and PGE2 synthesis. MK-886 51-56 prostaglandin E synthase Mus musculus 74-81 22038016-4 2011 Cytotoxicity assays and flow cytometry showed that MK886, an inhibitor of mPGES-1, inhibits proliferation of HL-60 cells and induces apoptosis in a dose- and time-dependent manner, which may result from down-regulation of mPGES-1 expression and PGE2 synthesis. MK-886 51-56 prostaglandin E synthase Mus musculus 222-229 20472647-7 2010 A PPARalpha agonist (WY14643; 1 microm) enhanced Ca(2+)-regulated exocytosis, and a PPARalpha blocker (MK886; 50 microm) abolished the enhancement of Ca(2+)-regulated exocytosis induced by AA, IDM, AACOCF(3) and WY14643. MK-886 103-108 peroxisome proliferator-activated receptor alpha Cavia porcellus 84-93 21643005-10 2011 Moreover, treatment of LM-MCF-7 cells with the specific 5-LOX inhibitor MK-886 (20-40 mumol/L) or 5-LOX siRNA (50-100 nmol/L) decreased the promoter activity of FASN. MK-886 72-78 arachidonate 5-lipoxygenase Homo sapiens 56-61 21643005-10 2011 Moreover, treatment of LM-MCF-7 cells with the specific 5-LOX inhibitor MK-886 (20-40 mumol/L) or 5-LOX siRNA (50-100 nmol/L) decreased the promoter activity of FASN. MK-886 72-78 lysyl oxidase Homo sapiens 58-61 21643005-10 2011 Moreover, treatment of LM-MCF-7 cells with the specific 5-LOX inhibitor MK-886 (20-40 mumol/L) or 5-LOX siRNA (50-100 nmol/L) decreased the promoter activity of FASN. MK-886 72-78 fatty acid synthase Homo sapiens 161-165 21602738-5 2011 Also, the effects of inhibition of LTB4 biosynthesis by pretreatment with the 5-lipoxygenase-activating peptide inhibitor, MK-886, were determined. MK-886 123-129 arachidonate 5-lipoxygenase Rattus norvegicus 78-92 21602738-9 2011 MK-886 pretreatment significantly inhibited pancreatic edema, histological damage, and pancreatic MPO concentrations. MK-886 0-6 myeloperoxidase Rattus norvegicus 98-101 21993002-4 2011 The present study provides evidence that combined use of celecoxib and 5-LOX inhibitor MK886 markedly suppresses pancreatic tumor cell growth in vitro. MK-886 87-92 arachidonate 5-lipoxygenase Homo sapiens 71-76 21993002-6 2011 We found that MK886 reversed celecoxib-induced increases in 5-LOX gene expression and Erk1/2 activation in pancreatic tumor cells. MK-886 14-19 arachidonate 5-lipoxygenase Homo sapiens 60-65 21993002-6 2011 We found that MK886 reversed celecoxib-induced increases in 5-LOX gene expression and Erk1/2 activation in pancreatic tumor cells. MK-886 14-19 mitogen-activated protein kinase 3 Homo sapiens 86-92 21993002-7 2011 Moreover, Dual treatment of pancreatic tumor cells with celecoxib and MK886 inhibited the levels of LBT4 receptor BLT1 and vascular endothelial growth factor. MK-886 70-75 leukotriene B4 receptor Homo sapiens 114-118 21993002-7 2011 Moreover, Dual treatment of pancreatic tumor cells with celecoxib and MK886 inhibited the levels of LBT4 receptor BLT1 and vascular endothelial growth factor. MK-886 70-75 vascular endothelial growth factor A Homo sapiens 123-157 21555210-5 2011 Although MK886 did not attenuate cuprizone-induced demyelination in the corpus callosum or in the cortex, it attenuated cuprizone-induced axonal damage and motor deficits and reduced microglial activation and IL-6 production. MK-886 9-14 interleukin 6 Mus musculus 209-213 21649921-10 2011 MK-886 also significantly decreased serum TNF-alpha & IL-6; lung MDA; BALF LTB4, LTC4 & total protein compared with the HS group (P < 0.05). MK-886 0-6 tumor necrosis factor Rattus norvegicus 42-51 21649921-10 2011 MK-886 also significantly decreased serum TNF-alpha & IL-6; lung MDA; BALF LTB4, LTC4 & total protein compared with the HS group (P < 0.05). MK-886 0-6 interleukin 6 Rattus norvegicus 58-62 21323895-6 2011 The inhibitory effect of 20-HETE on COX-2 expression was mimicked by WY14643, a PPARalpha ligand and inhibited by MK886, a PPARalpha inhibitor or by transfection of shRNA for PPARalpha. MK-886 114-119 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 36-41 21323895-6 2011 The inhibitory effect of 20-HETE on COX-2 expression was mimicked by WY14643, a PPARalpha ligand and inhibited by MK886, a PPARalpha inhibitor or by transfection of shRNA for PPARalpha. MK-886 114-119 peroxisome proliferator activated receptor alpha Rattus norvegicus 123-132 21323895-6 2011 The inhibitory effect of 20-HETE on COX-2 expression was mimicked by WY14643, a PPARalpha ligand and inhibited by MK886, a PPARalpha inhibitor or by transfection of shRNA for PPARalpha. MK-886 114-119 peroxisome proliferator activated receptor alpha Rattus norvegicus 123-132 21323895-8 2011 Furthermore, ATPgammaS-induced activation of the COX-2 promoter containing the activated protein-1 site was also inhibited by pretreatment with 20-HETE, which was reversed by MK886 or by transfection with shRNA for PPARalpha. MK-886 175-180 prostaglandin-endoperoxide synthase 2 Rattus norvegicus 49-54 21645444-1 2011 OBJECTIVE: To study the expression of mPGES-1 in hepatocellular carcinoma (HCC), observe the effect of MK886 on down-regulation of mPGES-1 gene expression on the biology of human hepatocarcinoma cell line HepG2 and to investigate its significance in the occurrence, progression, metastasis and invasion. MK-886 103-108 prostaglandin E synthase Mus musculus 131-138 21435438-9 2011 The inhibition of PPAR-alpha by its inhibitor, MK886, or knockdown of PPAR-alpha by small interfering RNA significantly inhibited the expression of TRB3 induced by homocysteine. MK-886 47-52 peroxisome proliferator activated receptor alpha Mus musculus 18-28 21435438-9 2011 The inhibition of PPAR-alpha by its inhibitor, MK886, or knockdown of PPAR-alpha by small interfering RNA significantly inhibited the expression of TRB3 induced by homocysteine. MK-886 47-52 tribbles pseudokinase 3 Mus musculus 148-152 20801430-7 2011 The ability of WY14643 and methOEA to counteract the behavioral, electrophysiological, and neurochemical effects of nicotine was reversed by the PPAR-alpha antagonist 1-[(4-Chlorophenyl)methyl]-3-[(1,1-dimethylethyl)thio]-a,a-dimethyl-5-(1-methylethyl)-1H-Indole-2-propanoic acid (MK886). MK-886 281-286 peroxisome proliferator activated receptor alpha Rattus norvegicus 145-155 21352343-6 2011 The effect of MK886, a 5-LOX-specific inhibitor, on the expression of TGF-beta1, CTGF, type I and type III collagen was also examined by RT-PCR. MK-886 14-19 transforming growth factor beta 1 Homo sapiens 70-79 21352343-6 2011 The effect of MK886, a 5-LOX-specific inhibitor, on the expression of TGF-beta1, CTGF, type I and type III collagen was also examined by RT-PCR. MK-886 14-19 cellular communication network factor 2 Homo sapiens 81-85 20521013-11 2010 Therefore, these data suggest that the production of IL-17 in MK-886-treated, immunized mice could contribute to the generation of a protective immune response after infection with M. tuberculosis. MK-886 62-68 interleukin 17A Mus musculus 53-58 19809821-6 2010 Furthermore, we examined the effects of leukotrienes synthesis inhibitors, MK886 and bestatin, on mRNA and protein levels of TNFalpha and IL1beta in RASF. MK-886 75-80 tumor necrosis factor Homo sapiens 125-133 20370567-4 2010 Linked to these results, HNE increased membrane translocation of p47phox promoting NADPH oxidase activity, which was attenuated in peritoneal macrophages from 5-LO-deficient mice as well as in J774A.1 cells treated with a 5-LO inhibitor, MK886 or 5-LO siRNA. MK-886 238-243 neutrophil cytosolic factor 1 Mus musculus 65-72 20042322-7 2010 And osthol-regulated mRNA expressions of DGAT, HMG-CoA reductase and CYP7A in the cultured hepatocytes were abrogated after pretreatment with specific inhibitor of PPAR alpha, MK886. MK-886 176-181 diacylglycerol O-acyltransferase 1 Mus musculus 41-45 19809821-6 2010 Furthermore, we examined the effects of leukotrienes synthesis inhibitors, MK886 and bestatin, on mRNA and protein levels of TNFalpha and IL1beta in RASF. MK-886 75-80 interleukin 1 beta Homo sapiens 138-145 20128796-5 2010 KEY RESULTS: In rat hippocampal slices, glutamate-induced excitotoxicity, as well as prostaglandin (PG) E(2) production and PGES activation, was significantly attenuated by either MK-886 or NS-398, inhibitors of mPGES-1 and COX-2 respectively; however, co-application of these inhibitors had neither an additive nor a synergistic effect. MK-886 180-186 prostaglandin E synthase Mus musculus 212-219 20061081-7 2010 MK886 (5-LOX activating protein inhibitor) mediated the induction of apoptosis by elevation of caspase-3 and Bax/Bcl2 ratio. MK-886 0-5 arachidonate 5-lipoxygenase Homo sapiens 7-12 20061081-7 2010 MK886 (5-LOX activating protein inhibitor) mediated the induction of apoptosis by elevation of caspase-3 and Bax/Bcl2 ratio. MK-886 0-5 caspase 3 Homo sapiens 95-104 20061081-7 2010 MK886 (5-LOX activating protein inhibitor) mediated the induction of apoptosis by elevation of caspase-3 and Bax/Bcl2 ratio. MK-886 0-5 BCL2 associated X, apoptosis regulator Homo sapiens 109-112 20061081-7 2010 MK886 (5-LOX activating protein inhibitor) mediated the induction of apoptosis by elevation of caspase-3 and Bax/Bcl2 ratio. MK-886 0-5 BCL2 apoptosis regulator Homo sapiens 113-117 20567598-3 2010 Here, we report the identification of the 5-lipoxygenase inhibitors, NDGA, AA861, and MK886, as potent blockers of the TRPM7 channel. MK-886 86-91 arachidonate 5-lipoxygenase Homo sapiens 42-56 20567598-3 2010 Here, we report the identification of the 5-lipoxygenase inhibitors, NDGA, AA861, and MK886, as potent blockers of the TRPM7 channel. MK-886 86-91 transient receptor potential cation channel subfamily M member 7 Homo sapiens 119-124 20173757-5 2010 Then, using the treatment with MK886, a specific 5-lipoxygenases (5-LOX) inhibitor, (or 5-LOX siRNA) we identified that 5-LOX was responsible for the upregulation of SREBP-1c by luciferase reporter gene assay, RT-PCR and Western blot analysis. MK-886 31-36 sterol regulatory element binding transcription factor 1 Homo sapiens 166-174 20364155-6 2010 And the effect of MK886, a specific inhibitor of 5-lipoxygenase (5-LOX), on OPN promoter activity and mRNA expression in HepG2-X Delta 127 and H7402-X Delta 127 cells were examined using luciferase reporter gene assays and RT-PCR, respectively. MK-886 18-23 arachidonate 5-lipoxygenase Homo sapiens 65-70 20364155-6 2010 And the effect of MK886, a specific inhibitor of 5-lipoxygenase (5-LOX), on OPN promoter activity and mRNA expression in HepG2-X Delta 127 and H7402-X Delta 127 cells were examined using luciferase reporter gene assays and RT-PCR, respectively. MK-886 18-23 secreted phosphoprotein 1 Homo sapiens 76-79 20364155-10 2010 Moreover, MK886 abolished the HBx Delta 127-mediated upregulation of OPN. MK-886 10-15 X protein Hepatitis B virus 30-33 20364155-10 2010 Moreover, MK886 abolished the HBx Delta 127-mediated upregulation of OPN. MK-886 10-15 secreted phosphoprotein 1 Homo sapiens 69-72 19896470-9 2010 These data illustrate that inhibition of sEH by both pharmacological intervention and gene knockout enhances the anti-inflammatory effects of aspirin and MK886, suggesting the possibility of modulating multiple branches to achieve better therapeutic effects. MK-886 154-159 epoxide hydrolase 2, cytoplasmic Mus musculus 41-44 20128796-5 2010 KEY RESULTS: In rat hippocampal slices, glutamate-induced excitotoxicity, as well as prostaglandin (PG) E(2) production and PGES activation, was significantly attenuated by either MK-886 or NS-398, inhibitors of mPGES-1 and COX-2 respectively; however, co-application of these inhibitors had neither an additive nor a synergistic effect. MK-886 180-186 cytochrome c oxidase II, mitochondrial Rattus norvegicus 224-229 20126469-7 2010 Moreover, we found that 5-lipoxygenase (5-LOX) was responsible for the up-regulation of FAS by using MK886 (an inhibitor of 5-LOX) and 5-LOX small interfering RNA. MK-886 101-106 arachidonate 5-lipoxygenase Homo sapiens 24-38 19938896-9 2010 Last, we found that MK-886, a known inhibitor of peroxisome proliferator-activated receptor alpha (PPARalpha), increased the MEHP-induced TNF-alpha response. MK-886 20-26 peroxisome proliferator activated receptor alpha Rattus norvegicus 49-97 19938896-9 2010 Last, we found that MK-886, a known inhibitor of peroxisome proliferator-activated receptor alpha (PPARalpha), increased the MEHP-induced TNF-alpha response. MK-886 20-26 peroxisome proliferator activated receptor alpha Rattus norvegicus 99-108 19938896-9 2010 Last, we found that MK-886, a known inhibitor of peroxisome proliferator-activated receptor alpha (PPARalpha), increased the MEHP-induced TNF-alpha response. MK-886 20-26 tumor necrosis factor Rattus norvegicus 138-147 19880577-6 2010 The in vivo inhibition of LTB(4) biosynthesis by the 5-LO inhibitor zileuton or the FLAP inhibitor MK886 attenuated LPS-induced gammadelta T cell accumulation into pleural cavities. MK-886 99-104 arachidonate 5-lipoxygenase activating protein Mus musculus 84-88 20126469-7 2010 Moreover, we found that 5-lipoxygenase (5-LOX) was responsible for the up-regulation of FAS by using MK886 (an inhibitor of 5-LOX) and 5-LOX small interfering RNA. MK-886 101-106 arachidonate 5-lipoxygenase Homo sapiens 40-45 20126469-7 2010 Moreover, we found that 5-lipoxygenase (5-LOX) was responsible for the up-regulation of FAS by using MK886 (an inhibitor of 5-LOX) and 5-LOX small interfering RNA. MK-886 101-106 fatty acid synthase Homo sapiens 88-91 20126469-7 2010 Moreover, we found that 5-lipoxygenase (5-LOX) was responsible for the up-regulation of FAS by using MK886 (an inhibitor of 5-LOX) and 5-LOX small interfering RNA. MK-886 101-106 lysyl oxidase Homo sapiens 42-45 20126469-7 2010 Moreover, we found that 5-lipoxygenase (5-LOX) was responsible for the up-regulation of FAS by using MK886 (an inhibitor of 5-LOX) and 5-LOX small interfering RNA. MK-886 101-106 lysyl oxidase Homo sapiens 126-129 19883121-6 2009 Treatment of HepG2 cells with PPARalpha antagonist (MK886) or LXR agonist (TO901317) abolishes the TNFalpha-mediated decrease in the level of apoA-I gene expression. MK-886 52-57 peroxisome proliferator activated receptor alpha Homo sapiens 30-39 19586628-3 2010 VSMC stimulated with HNE (1 microM) produced MMP-2, which was markedly attenuated in 5-LO-deficient VSMC as well as in cells pretreated with a FLAP inhibitor, MK886, confirming a role for 5-LO metabolites in HNE-enhanced MMP-2 production. MK-886 159-164 matrix metallopeptidase 2 Homo sapiens 45-50 19586628-3 2010 VSMC stimulated with HNE (1 microM) produced MMP-2, which was markedly attenuated in 5-LO-deficient VSMC as well as in cells pretreated with a FLAP inhibitor, MK886, confirming a role for 5-LO metabolites in HNE-enhanced MMP-2 production. MK-886 159-164 matrix metallopeptidase 2 Homo sapiens 221-226 19683050-5 2010 Bezafibrate at toxic doses of 300 and 1000microM upregulated PPARalpha at the mRNA level, counteracted by a PPARalpha antagonist (MK886). MK-886 130-135 peroxisome proliferator activated receptor alpha Homo sapiens 61-70 19683050-5 2010 Bezafibrate at toxic doses of 300 and 1000microM upregulated PPARalpha at the mRNA level, counteracted by a PPARalpha antagonist (MK886). MK-886 130-135 peroxisome proliferator activated receptor alpha Homo sapiens 108-117 19837106-4 2010 This was associated with an increased production of MMP-9, which was blunted by inhibition of 5-LO with MK886, a 5-LO inhibitor or with 5-LO siRNA. MK-886 104-109 matrix metallopeptidase 9 Mus musculus 52-57 19883121-6 2009 Treatment of HepG2 cells with PPARalpha antagonist (MK886) or LXR agonist (TO901317) abolishes the TNFalpha-mediated decrease in the level of apoA-I gene expression. MK-886 52-57 tumor necrosis factor Homo sapiens 99-107 19883121-6 2009 Treatment of HepG2 cells with PPARalpha antagonist (MK886) or LXR agonist (TO901317) abolishes the TNFalpha-mediated decrease in the level of apoA-I gene expression. MK-886 52-57 apolipoprotein A1 Homo sapiens 142-148 19876784-4 2009 FLAP inhibitors such as MK-886, MK-0591 and veliflapon (BAY-X-1005, DG-031) demonstrated promise in clinical trials with patients with inflammatory diseases in the mid 1990 s, but, unlike the "lukast" class of cysteinyl-leukotriene receptor antagonists, these compounds were not brought to market. MK-886 24-30 arachidonate 5-lipoxygenase activating protein Homo sapiens 0-4 20193367-11 2009 These effects of fenofibrate were abolished by PPARalpha inhibitor MK886, suggesting that fenofibrate activated through PPARalpha. MK-886 67-72 peroxisome proliferator activated receptor alpha Rattus norvegicus 47-56 20193367-11 2009 These effects of fenofibrate were abolished by PPARalpha inhibitor MK886, suggesting that fenofibrate activated through PPARalpha. MK-886 67-72 peroxisome proliferator activated receptor alpha Rattus norvegicus 120-129 19371256-0 2009 Effect of MK-886 on Ca2+ level and viability in PC3 human prostate cancer cells. MK-886 10-16 chromobox 8 Homo sapiens 48-51 19877201-11 2009 A20-mediated protection of hepatocytes from hypoxia/reoxygenation and H(2)O(2)-mediated necrosis was reverted by pretreatment with the PPARalpha inhibitor MK886. MK-886 155-160 tumor necrosis factor, alpha-induced protein 3 Mus musculus 0-3 19877201-11 2009 A20-mediated protection of hepatocytes from hypoxia/reoxygenation and H(2)O(2)-mediated necrosis was reverted by pretreatment with the PPARalpha inhibitor MK886. MK-886 155-160 peroxisome proliferator activated receptor alpha Mus musculus 135-144 19694729-11 2009 Adding an inhibitor of PPARalpha (MK886) abolished the effects of atorvastatin on HepG2 cells. MK-886 34-39 peroxisome proliferator activated receptor alpha Homo sapiens 23-32 19220423-3 2009 We demonstrated previously that the co-treatment of HL-60 cells with Tumor necrosis factor-alpha (TNF-alpha) (1 ng/mL) and inhibitor of 5-lipoxygenase MK886 (5 microm) potentiated both monocytic differentiation and apoptosis. MK-886 151-156 tumor necrosis factor Homo sapiens 98-107 19220423-5 2009 The inhibition of pro-apoptotic MAPKs (p38 and JNK) suppressed the effect of MK886 + TNF-alpha co-treatment. MK-886 77-82 mitogen-activated protein kinase 14 Homo sapiens 39-42 19220423-5 2009 The inhibition of pro-apoptotic MAPKs (p38 and JNK) suppressed the effect of MK886 + TNF-alpha co-treatment. MK-886 77-82 mitogen-activated protein kinase 8 Homo sapiens 47-50 19220423-5 2009 The inhibition of pro-apoptotic MAPKs (p38 and JNK) suppressed the effect of MK886 + TNF-alpha co-treatment. MK-886 77-82 tumor necrosis factor Homo sapiens 85-94 19220423-7 2009 Those effects were accompanied by increased activation of caspases in cells treated by MK886 + TNF-alpha. MK-886 87-92 caspase 8 Homo sapiens 58-66 19425605-7 2009 Inclusion of the PPARalpha inhibitor, MK-886, or MAPK inhibitor, U0126, completely blocks the LAPL-induced apoA-I and HL accumulation in the media. MK-886 38-44 apolipoprotein A1 Homo sapiens 107-113 19425605-7 2009 Inclusion of the PPARalpha inhibitor, MK-886, or MAPK inhibitor, U0126, completely blocks the LAPL-induced apoA-I and HL accumulation in the media. MK-886 38-44 lipase C, hepatic type Homo sapiens 118-120 19415458-3 2009 These VD3 effects on HL-60 cell differentiation were significantly potentiated by 5-LPO inhibitors MK-886 and AA-861 and were inverted by SB202190 (SB), a p38 MAPK inhibitor. MK-886 99-105 lactoperoxidase Homo sapiens 84-87 19737966-4 2009 Inhibition of 5-lipoxygenase (5-LOX) seems to have a pivotal role in this model because caffeic acid and MK886, a FLAP (5-LOX-activating protein) inhibitor, partially hindered tumor growth induced by apoptotic cells or LPS. MK-886 105-110 arachidonate 5-lipoxygenase Mus musculus 14-28 19737966-4 2009 Inhibition of 5-lipoxygenase (5-LOX) seems to have a pivotal role in this model because caffeic acid and MK886, a FLAP (5-LOX-activating protein) inhibitor, partially hindered tumor growth induced by apoptotic cells or LPS. MK-886 105-110 lysyl oxidase Mus musculus 32-35 19737966-4 2009 Inhibition of 5-lipoxygenase (5-LOX) seems to have a pivotal role in this model because caffeic acid and MK886, a FLAP (5-LOX-activating protein) inhibitor, partially hindered tumor growth induced by apoptotic cells or LPS. MK-886 105-110 lysyl oxidase Mus musculus 122-125 19285113-14 2009 The central administration of MK-886 increased the hypothalamic LTC(4) synthase content but did not alter the plasma and neurohypophysis AVP levels observed, or the blood pressure during this phase. MK-886 30-36 leukotriene C4 synthase Rattus norvegicus 64-79 19371256-12 2009 Together, in PC3 cells, MK-886 induced [Ca(2+)](i) rises by causing phospholipase C-independent Ca(2+) release from the endoplasmic reticulum; and Ca(2+) influx via store-operated Ca(2+) channels. MK-886 24-30 chromobox 8 Homo sapiens 13-16 18656901-4 2009 MK-886 is an inhibitor of 5-lipoxygenase, and montelukast is a cysteinyl leukotriene receptor antagonist. MK-886 0-6 arachidonate 5-lipoxygenase Rattus norvegicus 26-40 19492148-10 2009 The decrease in PAI-1 expression induced by gemfibrozil was inhibited by MK886, a PPARalpha inhibitor. MK-886 73-78 serine (or cysteine) peptidase inhibitor, clade E, member 1 Mus musculus 16-21 19492148-10 2009 The decrease in PAI-1 expression induced by gemfibrozil was inhibited by MK886, a PPARalpha inhibitor. MK-886 73-78 peroxisome proliferator activated receptor alpha Mus musculus 82-91 19403796-2 2009 Using a passive-avoidance task in rats, we found that memory acquisition was enhanced by the FAAH inhibitor URB597 or by the PPAR-alpha agonist WY14643, and these enhancements were blocked by the PPAR-alpha antagonist MK886. MK-886 218-223 fatty-acid amide hydrolase-like Rattus norvegicus 93-97 19403796-2 2009 Using a passive-avoidance task in rats, we found that memory acquisition was enhanced by the FAAH inhibitor URB597 or by the PPAR-alpha agonist WY14643, and these enhancements were blocked by the PPAR-alpha antagonist MK886. MK-886 218-223 peroxisome proliferator activated receptor alpha Rattus norvegicus 125-135 19403796-2 2009 Using a passive-avoidance task in rats, we found that memory acquisition was enhanced by the FAAH inhibitor URB597 or by the PPAR-alpha agonist WY14643, and these enhancements were blocked by the PPAR-alpha antagonist MK886. MK-886 218-223 peroxisome proliferator activated receptor alpha Rattus norvegicus 196-206 19239910-0 2009 MK-886, an inhibitor of the 5-lipoxygenase-activating protein, inhibits cyclooxygenase-1 activity and suppresses platelet aggregation. MK-886 0-6 arachidonate 5-lipoxygenase Homo sapiens 28-42 19239910-0 2009 MK-886, an inhibitor of the 5-lipoxygenase-activating protein, inhibits cyclooxygenase-1 activity and suppresses platelet aggregation. MK-886 0-6 prostaglandin-endoperoxide synthase 1 Homo sapiens 72-88 19239910-5 2009 The distinct susceptibility of MK-886 towards COX-1 and -2 is apparent in automated molecular docking studies that indicate a preferred binding of MK-886 to COX-1 into the active site. MK-886 31-37 mitochondrially encoded cytochrome c oxidase I Homo sapiens 46-58 19239910-5 2009 The distinct susceptibility of MK-886 towards COX-1 and -2 is apparent in automated molecular docking studies that indicate a preferred binding of MK-886 to COX-1 into the active site. MK-886 31-37 mitochondrially encoded cytochrome c oxidase I Homo sapiens 46-51 19239910-5 2009 The distinct susceptibility of MK-886 towards COX-1 and -2 is apparent in automated molecular docking studies that indicate a preferred binding of MK-886 to COX-1 into the active site. MK-886 147-153 mitochondrially encoded cytochrome c oxidase I Homo sapiens 46-58 19239910-5 2009 The distinct susceptibility of MK-886 towards COX-1 and -2 is apparent in automated molecular docking studies that indicate a preferred binding of MK-886 to COX-1 into the active site. MK-886 147-153 mitochondrially encoded cytochrome c oxidase I Homo sapiens 46-51 19239910-6 2009 MK-886 (10 microM) inhibited COX-1-mediated platelet aggregation induced by collagen or arachidonic acid whereas thrombin- or U-46619-induced (COX-independent) aggregation was not affected. MK-886 0-6 mitochondrially encoded cytochrome c oxidase I Homo sapiens 29-34 19239910-1 2009 MK-886, an inhibitor of the 5-lipoxygenase-activating protein (FLAP), potently suppresses leukotriene biosynthesis in intact cells and is frequently used to define a role of the 5-lipoxygenase (EC 1.13.11.34) pathway in cellular or animal models of inflammation, allergy, cancer, and cardiovascular disease. MK-886 0-6 arachidonate 5-lipoxygenase Homo sapiens 28-42 19239910-1 2009 MK-886, an inhibitor of the 5-lipoxygenase-activating protein (FLAP), potently suppresses leukotriene biosynthesis in intact cells and is frequently used to define a role of the 5-lipoxygenase (EC 1.13.11.34) pathway in cellular or animal models of inflammation, allergy, cancer, and cardiovascular disease. MK-886 0-6 arachidonate 5-lipoxygenase activating protein Homo sapiens 63-67 19239910-1 2009 MK-886, an inhibitor of the 5-lipoxygenase-activating protein (FLAP), potently suppresses leukotriene biosynthesis in intact cells and is frequently used to define a role of the 5-lipoxygenase (EC 1.13.11.34) pathway in cellular or animal models of inflammation, allergy, cancer, and cardiovascular disease. MK-886 0-6 arachidonate 5-lipoxygenase Homo sapiens 178-192 19239910-3 2009 MK-886 inhibited isolated COX-1 (IC(50)=8 microM) and blocked the formation of the COX-1-derived products 12(S)-hydroxy-5-cis-8,10-trans-heptadecatrienoic acid (12-HHT) and thromboxane B(2) in washed human platelets in response to collagen as well as from exogenous arachidonic acid (IC(50)=13-15 microM). MK-886 0-6 mitochondrially encoded cytochrome c oxidase I Homo sapiens 26-31 19239910-3 2009 MK-886 inhibited isolated COX-1 (IC(50)=8 microM) and blocked the formation of the COX-1-derived products 12(S)-hydroxy-5-cis-8,10-trans-heptadecatrienoic acid (12-HHT) and thromboxane B(2) in washed human platelets in response to collagen as well as from exogenous arachidonic acid (IC(50)=13-15 microM). MK-886 0-6 mitochondrially encoded cytochrome c oxidase I Homo sapiens 83-88 18842827-9 2008 The increase in PGE(2) production subsequently stimulated peroxisome proliferator-activated receptor (PPAR) expression, and MK-886 (PPAR-alpha antagonist) and GW-9662 (PPAR-delta antagonist) inhibited glucose-6-phosphatase and phosphoenolpyruvate carboxykinase. MK-886 124-130 peroxisome proliferator activated receptor alpha Gallus gallus 132-142 19289819-7 2009 IL-17-induced neutrophil migration was not affected by COX inhibitors, IL-12, or IFNgamma but was inhibited by MK886 (a leukotriene synthesis inhibitor), anti-TNFalpha, anti-CXCL1, and anti-CXCL5 antibodies and by repertaxin (a CXCR1/2 antagonist). MK-886 111-116 interleukin 17A Mus musculus 0-5 18403121-2 2008 Increased activity of the enzymatic 5-lipoxygenase (5-LOX, 5LO) pathway is a contributing factor in atherosclerosis and a 5-LOX inhibitor, MK-886, is beneficial in animal models of atherosclerosis. MK-886 139-145 arachidonate 5-lipoxygenase Mus musculus 36-50 18771933-1 2008 In our previous study we have proved that colon cancer cells HT-29 pre-treated with specific 5-lipoxygenase inhibitor MK-886 became more susceptible to photodynamic therapy (PDT) with hypericin and we also found that this mutual combination induced cell cycle arrest and stimulated onset of apoptosis (Kleban et al., 2007. MK-886 118-124 arachidonate 5-lipoxygenase Homo sapiens 93-107 18601933-5 2008 Eosinophil recruitment required Major Histocompatibility Complex Class II expression, and was abolished by the leukotriene B4 (LTB4) receptor antagonist CP 105.696, the 5-lipoxygenase inhibitor BWA4C and the 5-lipoxygenase activating protein inhibitor MK886. MK-886 252-257 leukotriene B4 receptor 1 Mus musculus 111-141 18601933-5 2008 Eosinophil recruitment required Major Histocompatibility Complex Class II expression, and was abolished by the leukotriene B4 (LTB4) receptor antagonist CP 105.696, the 5-lipoxygenase inhibitor BWA4C and the 5-lipoxygenase activating protein inhibitor MK886. MK-886 252-257 arachidonate 5-lipoxygenase Mus musculus 208-222 18601933-10 2008 MK886 blocked induction of CCL17. MK-886 0-5 chemokine (C-C motif) ligand 17 Mus musculus 27-32 18601933-11 2008 Pretreatment of EWI carriers with MK886 eliminated the effectiveness of exogenously administered CCL11, CCL2 and CCL5. MK-886 34-39 chemokine (C-C motif) ligand 11 Mus musculus 97-102 18601933-11 2008 Pretreatment of EWI carriers with MK886 eliminated the effectiveness of exogenously administered CCL11, CCL2 and CCL5. MK-886 34-39 chemokine (C-C motif) ligand 2 Mus musculus 104-108 18601933-11 2008 Pretreatment of EWI carriers with MK886 eliminated the effectiveness of exogenously administered CCL11, CCL2 and CCL5. MK-886 34-39 chemokine (C-C motif) ligand 5 Mus musculus 113-117 18576322-9 2008 Repertaxin reduced LTB4 production in joint tissue, and neutrophil recruitment induced by CXCL1 or CXCL5 was inhibited by MK886, suggesting a sequential mechanism. MK-886 122-127 chemokine (C-X-C motif) ligand 1 Mus musculus 90-95 18576322-9 2008 Repertaxin reduced LTB4 production in joint tissue, and neutrophil recruitment induced by CXCL1 or CXCL5 was inhibited by MK886, suggesting a sequential mechanism. MK-886 122-127 chemokine (C-X-C motif) ligand 5 Mus musculus 99-104 18710415-10 2008 The protective effects of PPAR over-expression were reversed by the antagonists of PPARalpha (MK886) or PPARgamma (GW9662). MK-886 94-99 peroxisome proliferator activated receptor alpha Homo sapiens 26-30 18710415-10 2008 The protective effects of PPAR over-expression were reversed by the antagonists of PPARalpha (MK886) or PPARgamma (GW9662). MK-886 94-99 peroxisome proliferator activated receptor alpha Homo sapiens 83-92 18953103-1 2008 We have shown that inhibitors of five lipoxygenase activating protein (FLAP)--MK-886 and BAYx1005 inhibit atherosclerosis in apolipoprotein E/LDL receptor-double knockout mice. MK-886 78-84 apolipoprotein E Mus musculus 125-141 18953103-1 2008 We have shown that inhibitors of five lipoxygenase activating protein (FLAP)--MK-886 and BAYx1005 inhibit atherosclerosis in apolipoprotein E/LDL receptor-double knockout mice. MK-886 78-84 low density lipoprotein receptor Mus musculus 142-154 18403121-2 2008 Increased activity of the enzymatic 5-lipoxygenase (5-LOX, 5LO) pathway is a contributing factor in atherosclerosis and a 5-LOX inhibitor, MK-886, is beneficial in animal models of atherosclerosis. MK-886 139-145 arachidonate 5-lipoxygenase Mus musculus 52-57 18403121-2 2008 Increased activity of the enzymatic 5-lipoxygenase (5-LOX, 5LO) pathway is a contributing factor in atherosclerosis and a 5-LOX inhibitor, MK-886, is beneficial in animal models of atherosclerosis. MK-886 139-145 arachidonate 5-lipoxygenase Mus musculus 122-127 18403121-3 2008 In the brain, MK-886 increases phosphorylation of the glutamate receptor subunit GluR1, and the increased phosphorylation of this receptor has been associated with antidepressant treatment. MK-886 14-20 glutamate receptor, ionotropic, AMPA1 (alpha 1) Mus musculus 81-86 18403121-5 2008 Whereas a single injection of MK-886 (3 and 10 mg/kg) did not affect forced swimming behaviors assayed 30 min later, six daily injections of 3 mg/kg MK-886 slightly increased climbing and significantly reduced rest time in wild-type mice but not in 5-LOX-deficient mice. MK-886 149-155 arachidonate 5-lipoxygenase Mus musculus 249-254 17707523-9 2007 Dexamethasone and MK-886 both inhibited the cytokine-induced mPGES-1 expression while mPGES-2 and cPGES expression remained unaffected. MK-886 18-24 prostaglandin E synthase Mus musculus 61-68 18292206-3 2008 In the present study, the application of reporter animal technology was instrumental to obtain the global pharmacological profiling indispensable to unraveling 3-(1-(4-chlorobenzyl)-3-t-butylthio-5-isopropylindol-2-yl)-2,2-dimethylpropanoic acid (MK-886)-selective PPAR modulator (SPPARM) activity not underlined by previous traditional, cell-based studies. MK-886 160-245 peroxisome proliferator activated receptor alpha Homo sapiens 265-269 18189424-8 2008 Pretreatment with the peroxisome proliferator-activated receptor alpha (PPARalpha) inhibitor MK886 (10 microM) also completely blocked PI- and DLPC-induced apoA-I secretion. MK-886 93-98 peroxisome proliferator activated receptor alpha Homo sapiens 22-70 18189424-8 2008 Pretreatment with the peroxisome proliferator-activated receptor alpha (PPARalpha) inhibitor MK886 (10 microM) also completely blocked PI- and DLPC-induced apoA-I secretion. MK-886 93-98 peroxisome proliferator activated receptor alpha Homo sapiens 72-81 18189424-8 2008 Pretreatment with the peroxisome proliferator-activated receptor alpha (PPARalpha) inhibitor MK886 (10 microM) also completely blocked PI- and DLPC-induced apoA-I secretion. MK-886 93-98 apolipoprotein A1 Homo sapiens 156-162 17991720-7 2008 Treatment with MK886 inhibited expression of PPARalpha, blocking PPARalpha-regulated PDX-1 expression, and the downstream transcription events of PDX-1. MK-886 15-20 peroxisome proliferator activated receptor alpha Rattus norvegicus 45-54 17991720-7 2008 Treatment with MK886 inhibited expression of PPARalpha, blocking PPARalpha-regulated PDX-1 expression, and the downstream transcription events of PDX-1. MK-886 15-20 peroxisome proliferator activated receptor alpha Rattus norvegicus 65-74 17991720-7 2008 Treatment with MK886 inhibited expression of PPARalpha, blocking PPARalpha-regulated PDX-1 expression, and the downstream transcription events of PDX-1. MK-886 15-20 pancreatic and duodenal homeobox 1 Rattus norvegicus 85-90 17991720-7 2008 Treatment with MK886 inhibited expression of PPARalpha, blocking PPARalpha-regulated PDX-1 expression, and the downstream transcription events of PDX-1. MK-886 15-20 pancreatic and duodenal homeobox 1 Rattus norvegicus 146-151 18028339-7 2008 In vitro pre-treatment of U87 glioma cells with MK-886, a specific 5-LOX inhibitor, significantly enhanced the antimitotic effect of CBD, whereas the pre-treatment with indomethacin (pan-COX inhibitor) or celecoxib (COX-2 inhibitor), did not alter CBD effect. MK-886 48-54 arachidonate 5-lipoxygenase Mus musculus 69-72 18028339-7 2008 In vitro pre-treatment of U87 glioma cells with MK-886, a specific 5-LOX inhibitor, significantly enhanced the antimitotic effect of CBD, whereas the pre-treatment with indomethacin (pan-COX inhibitor) or celecoxib (COX-2 inhibitor), did not alter CBD effect. MK-886 48-54 cytochrome c oxidase II, mitochondrial Mus musculus 216-221 18187210-5 2008 FLAP was molecularly identified via a photoaffinity probe and an affinity gel based on MK-886, a selective leukotriene inhibitor that has no activity against broken-cell preparations of 5-LO. MK-886 87-93 arachidonate 5-lipoxygenase activating protein Homo sapiens 0-4 17979156-4 2007 IL-15-induced neutrophil migration was inhibited by anti-MIP-2 (CXCL2) antibody or MK886 (leukotriene synthesis inhibitor). MK-886 83-88 interleukin 15 Mus musculus 0-5 17872455-8 2007 The pioglitazone-induced apoA-I secretion or mRNA expression by the HepG2 cells was abrogated with the suppression of PPAR-alpha by small interfering RNA or a specific inhibitor of PPAR-alpha, MK886. MK-886 193-198 apolipoprotein A1 Homo sapiens 25-31 17872455-8 2007 The pioglitazone-induced apoA-I secretion or mRNA expression by the HepG2 cells was abrogated with the suppression of PPAR-alpha by small interfering RNA or a specific inhibitor of PPAR-alpha, MK886. MK-886 193-198 peroxisome proliferator activated receptor alpha Homo sapiens 118-128 18267115-8 2008 These effects of fenofibrate were abolished by PPARalpha inhibitor MK886, suggesting that fenofibrate activated through PPARalpha. MK-886 67-72 peroxisome proliferator activated receptor alpha Rattus norvegicus 47-56 18267115-8 2008 These effects of fenofibrate were abolished by PPARalpha inhibitor MK886, suggesting that fenofibrate activated through PPARalpha. MK-886 67-72 peroxisome proliferator activated receptor alpha Rattus norvegicus 120-129 17874178-5 2008 The chemotactic activity of the supernatant of IL-1beta-stimulated macrophages is due to the presence of LTB(4), since MK 886 inhibited its release. MK-886 119-125 interleukin 1 beta Rattus norvegicus 47-55 17913976-3 2008 It was observed that zymosan-induced articular hypernociception and neutrophil migration were reduced dose-dependently by the pretreatment with MK886 (1-9 mg/kg; LT synthesis inhibitor) as well as in 5-lypoxygenase-deficient mice (5LO(-/-)) or by the selective antagonist of the LTB(4) receptor (CP105696; 3 mg/kg). MK-886 144-149 leukotriene B4 receptor 1 Mus musculus 279-294 17951219-6 2008 In contrast, the PPARalpha antagonist MK886 decreased cardiomyogenesis, whereas the PPARbeta agonist L-165,041 as well as the PPARgamma agonist GW1929 were without effects. MK-886 38-43 peroxisome proliferator activated receptor alpha Mus musculus 17-26 17951219-7 2008 Treatment with PPARalpha, but not PPARbeta, and PPARgamma agonists and MK886, resulted in generation of reactive oxygen species (ROS), which was inhibited in the presence of the NADPH oxidase inhibitors diphenylen iodonium (DPI) and apocynin and the free radical scavengers vitamin E and N-(2-mercapto-propionyl)-glycine (NMPG), whereas the mitochondrial complex I inhibitor rotenone was without effects. MK-886 71-76 peroxisome proliferator activated receptor alpha Mus musculus 15-24 17928652-1 2007 Recently, we have shown that MK-886 - an inhibitor of five lipoxygenase activating protein (FLAP) inhibits atherosclerosis in apolipoprotein E / LDL receptor - double knockout mice. MK-886 29-35 arachidonate 5-lipoxygenase activating protein Mus musculus 92-96 17928652-1 2007 Recently, we have shown that MK-886 - an inhibitor of five lipoxygenase activating protein (FLAP) inhibits atherosclerosis in apolipoprotein E / LDL receptor - double knockout mice. MK-886 29-35 apolipoprotein E Mus musculus 126-142 17928652-1 2007 Recently, we have shown that MK-886 - an inhibitor of five lipoxygenase activating protein (FLAP) inhibits atherosclerosis in apolipoprotein E / LDL receptor - double knockout mice. MK-886 29-35 low density lipoprotein receptor Mus musculus 145-157 17558434-8 2007 The peroxisome proliferator-activated receptor-alpha antagonist, MK-886 (1 mg kg(-1)), partially attenuated the effect of L-29 on hypersensitivity in the PSNI model. MK-886 65-71 peroxisome proliferator activated receptor alpha Homo sapiens 4-52 17573087-6 2007 MK886 (PPARalpha antagonist) or PPARalpha knock-down by RNA interference (RNAi) inhibited PPARalpha activity as shown by the peroxisome proliferator response element-luciferase reporter assay, but only partially decreased up-regulation of UCP-2. MK-886 0-5 peroxisome proliferator activated receptor alpha Homo sapiens 7-16 17573087-6 2007 MK886 (PPARalpha antagonist) or PPARalpha knock-down by RNA interference (RNAi) inhibited PPARalpha activity as shown by the peroxisome proliferator response element-luciferase reporter assay, but only partially decreased up-regulation of UCP-2. MK-886 0-5 uncoupling protein 2 Homo sapiens 239-244 17558434-8 2007 The peroxisome proliferator-activated receptor-alpha antagonist, MK-886 (1 mg kg(-1)), partially attenuated the effect of L-29 on hypersensitivity in the PSNI model. MK-886 65-71 ribosomal protein L29 Homo sapiens 122-126 17349982-0 2007 5-Lipoxygenase inhibitor MK-886 increases GluR1 phosphorylation in neuronal cultures in vitro and in the mouse cortex in vivo. MK-886 25-31 arachidonate 5-lipoxygenase Mus musculus 0-14 17434475-11 2007 Furthermore, Gypenoside XLIX-induced inhibition on TNF-alpha-stimulated VCAM-1 promoter hyperactivity was completely abolished by a selective blocker of PPAR-alpha, MK-886. MK-886 165-171 tumor necrosis factor Homo sapiens 51-60 17434475-11 2007 Furthermore, Gypenoside XLIX-induced inhibition on TNF-alpha-stimulated VCAM-1 promoter hyperactivity was completely abolished by a selective blocker of PPAR-alpha, MK-886. MK-886 165-171 vascular cell adhesion molecule 1 Homo sapiens 72-78 17434475-11 2007 Furthermore, Gypenoside XLIX-induced inhibition on TNF-alpha-stimulated VCAM-1 promoter hyperactivity was completely abolished by a selective blocker of PPAR-alpha, MK-886. MK-886 165-171 peroxisome proliferator activated receptor alpha Homo sapiens 153-163 17349982-0 2007 5-Lipoxygenase inhibitor MK-886 increases GluR1 phosphorylation in neuronal cultures in vitro and in the mouse cortex in vivo. MK-886 25-31 glutamate receptor, ionotropic, AMPA1 (alpha 1) Mus musculus 42-47 17349982-2 2007 Previous in vitro studies in brain slices employed MK-886, a functional inhibitor of the enzyme 5-lipoxygenase (5-LOX), and found increased GluR1 phosphorylation. MK-886 51-57 arachidonate 5-lipoxygenase Mus musculus 96-110 17349982-2 2007 Previous in vitro studies in brain slices employed MK-886, a functional inhibitor of the enzyme 5-lipoxygenase (5-LOX), and found increased GluR1 phosphorylation. MK-886 51-57 arachidonate 5-lipoxygenase Mus musculus 112-117 17349982-2 2007 Previous in vitro studies in brain slices employed MK-886, a functional inhibitor of the enzyme 5-lipoxygenase (5-LOX), and found increased GluR1 phosphorylation. MK-886 51-57 glutamate receptor, ionotropic, AMPA1 (alpha 1) Mus musculus 140-145 17349982-3 2007 Since slice preparations have accompanying postmortem phosphorylation changes, e.g., decreased GluR1 phosphorylation, it remains to be clarified whether MK-886 can affect GluR1 phosphorylation in intact neurons and in the brain in vivo. MK-886 153-159 glutamate receptor, ionotropic, AMPA1 (alpha 1) Mus musculus 171-176 17349982-4 2007 We used primary neuronal cultures prepared from embryonic mouse brain and in vivo drug administration to investigate the effects of MK-886 on GluR1 phosphorylation using quantitative Western immunoblotting assays. MK-886 132-138 glutamate receptor, ionotropic, AMPA1 (alpha 1) Mus musculus 142-147 17349982-5 2007 In vitro, MK-886 increased GluR1 phosphorylation at both serine 831 and serine 845. MK-886 10-16 glutamate receptor, ionotropic, AMPA1 (alpha 1) Mus musculus 27-32 17349982-6 2007 In vivo, repeated but not a single MK-886 injection increased GluR1 phosphorylation in the prefrontal cortex. MK-886 35-41 glutamate receptor, ionotropic, AMPA1 (alpha 1) Mus musculus 62-67 17349982-7 2007 These findings indicate that MK-886 has an intrinsic effect on neuronal phosphorylation both in vitro and in vivo and support the use of MK-886 as a pharmacological tool in studies of not only the 5-LOX pathway but also neuronal GluR1 functioning. MK-886 29-35 arachidonate 5-lipoxygenase Mus musculus 197-202 17349982-7 2007 These findings indicate that MK-886 has an intrinsic effect on neuronal phosphorylation both in vitro and in vivo and support the use of MK-886 as a pharmacological tool in studies of not only the 5-LOX pathway but also neuronal GluR1 functioning. MK-886 29-35 glutamate receptor, ionotropic, AMPA1 (alpha 1) Mus musculus 229-234 17319946-7 2007 Nordihydroguaiaretic acid (NDGA), a non-selective lipoxygenase inhibitor, and MK886, a specific inhibitor of 5-lipoxygenase, induced MMP-3 expression synergistically with IL-1. MK-886 78-83 arachidonate 5-lipoxygenase Homo sapiens 109-123 17379835-7 2007 Four weeks of treatment with the FLAP inhibitor MK-886 (10 mg/kg in 1% tylose delivered by osmotic pumps) significantly reduced atherosclerotic lesion size and T-cell content. MK-886 48-54 arachidonate 5-lipoxygenase activating protein Mus musculus 33-37 17319946-7 2007 Nordihydroguaiaretic acid (NDGA), a non-selective lipoxygenase inhibitor, and MK886, a specific inhibitor of 5-lipoxygenase, induced MMP-3 expression synergistically with IL-1. MK-886 78-83 matrix metallopeptidase 3 Homo sapiens 133-138 17319946-7 2007 Nordihydroguaiaretic acid (NDGA), a non-selective lipoxygenase inhibitor, and MK886, a specific inhibitor of 5-lipoxygenase, induced MMP-3 expression synergistically with IL-1. MK-886 78-83 interleukin 1 alpha Homo sapiens 171-175 17319946-8 2007 However IL-4 was still able to inhibit MMP-3 expression in the presence of NDGA or MK886 and IL-1. MK-886 83-88 interleukin 4 Homo sapiens 8-12 17319946-8 2007 However IL-4 was still able to inhibit MMP-3 expression in the presence of NDGA or MK886 and IL-1. MK-886 83-88 matrix metallopeptidase 3 Homo sapiens 39-44 17949236-0 2007 Down-regulation of vinculin upon MK886-induced apoptosis in LN18 glioblastoma cells. MK-886 33-38 vinculin Homo sapiens 19-27 17552358-2 2007 Recently, COX-2 inhibitors (e.g.; celecoxib) and 5-LOX inhibitors (e.g.; MK886 and REV5901) used as single agents have shown promising activities in the treatment and chemoprevention of cancer. MK-886 73-78 lysyl oxidase Homo sapiens 51-54 17949236-3 2007 MK886 is a drug known to inhibit both 5- lipoxygenase-activating-protein (FLAP) and peroxisome proliferator activated receptor-alpha (PPAR-alpha). MK-886 0-5 arachidonate 5-lipoxygenase activating protein Homo sapiens 74-78 17949236-3 2007 MK886 is a drug known to inhibit both 5- lipoxygenase-activating-protein (FLAP) and peroxisome proliferator activated receptor-alpha (PPAR-alpha). MK-886 0-5 peroxisome proliferator activated receptor alpha Homo sapiens 84-132 17121918-0 2006 Inhibition of 5-lipoxygenase by MK886 augments the antitumor activity of celecoxib in human colon cancer cells. MK-886 32-37 arachidonate 5-lipoxygenase Homo sapiens 14-28 17949236-3 2007 MK886 is a drug known to inhibit both 5- lipoxygenase-activating-protein (FLAP) and peroxisome proliferator activated receptor-alpha (PPAR-alpha). MK-886 0-5 peroxisome proliferator activated receptor alpha Homo sapiens 134-144 17949236-10 2007 In addition, MK886-induced apoptosis in LN18 cells was accompanied by a decrease in the protein and mRNA levels of vinculin, but not other focal adhesion proteins. MK-886 13-18 vinculin Homo sapiens 115-123 17949236-11 2007 In summary, the data presented here indicate that disruption of the actin-vinculin-cell-cytoskeleton matrix of the LN18 glioblastoma is a component of the MK886 induced apoptosis. MK-886 155-160 vinculin Homo sapiens 74-82 17949236-12 2007 In addition, MK886 treated LN18 cells could provide one model in which to investigate drugs that target lipoxygenase and PPAR-alpha pathways in the chemotherapeutic treatment of glioblastomas. MK-886 13-18 peroxisome proliferator activated receptor alpha Homo sapiens 121-131 17047030-9 2007 The PPARalpha antagonist, MK-886, significantly suppressed PFOA and PFOS activity of mouse and human PPARalpha. MK-886 26-32 peroxisome proliferator activated receptor alpha Mus musculus 4-13 17047030-9 2007 The PPARalpha antagonist, MK-886, significantly suppressed PFOA and PFOS activity of mouse and human PPARalpha. MK-886 26-32 peroxisome proliferator activated receptor alpha Homo sapiens 101-110 17141290-9 2007 Furthermore, the Gyp XLIX-induced inhibitory effect on TF luciferase activity was completely abolished in the presence of the PPAR-alpha selective antagonist MK-886. MK-886 158-164 peroxisome proliferator activated receptor alpha Homo sapiens 126-136 17121918-9 2006 Combined treatment with 10 micromol/L celecoxib and MK886 could prevent this activation and had additive effects on inhibiting tumor cell proliferation, inducing cell apoptosis, decreasing Bcl-2 expression, increasing Bax expression, and determining mitochondrial depolarization in comparison with treatment with either inhibitor alone. MK-886 52-57 BCL2 apoptosis regulator Homo sapiens 189-194 17121918-9 2006 Combined treatment with 10 micromol/L celecoxib and MK886 could prevent this activation and had additive effects on inhibiting tumor cell proliferation, inducing cell apoptosis, decreasing Bcl-2 expression, increasing Bax expression, and determining mitochondrial depolarization in comparison with treatment with either inhibitor alone. MK-886 52-57 BCL2 associated X, apoptosis regulator Homo sapiens 218-221 17121918-11 2006 In conclusion, our study showed that inhibition of 5-LOX by MK886 could augment the antitumor activity of celecoxib in human colorectal cancer. MK-886 60-65 lysyl oxidase Homo sapiens 53-56 16863991-6 2006 The PPAR-alpha antagonist MK886 abolished the beneficial effects of WY14643. MK-886 26-31 peroxisome proliferator activated receptor alpha Rattus norvegicus 4-14 16782780-4 2006 This response was mediated by PPARalpha since it was blocked by MK886, a selective PPARalpha antagonist. MK-886 64-69 peroxisome proliferator activated receptor alpha Homo sapiens 30-39 16782780-4 2006 This response was mediated by PPARalpha since it was blocked by MK886, a selective PPARalpha antagonist. MK-886 64-69 peroxisome proliferator activated receptor alpha Homo sapiens 83-92 17068631-6 2006 LIT-treated synoviocytes with addition of MK-886 (5-LOX exciting protein FLAP inhibitor) (1-10 micromol/L) were inhibited to secrete LTB4 dose-dependently, following the markedly down-regulated expressions of TNF-alpha (15%-66%) and IL-1beta (41%-71%) at mRNA level . MK-886 42-48 tumor necrosis factor Homo sapiens 209-218 17068631-6 2006 LIT-treated synoviocytes with addition of MK-886 (5-LOX exciting protein FLAP inhibitor) (1-10 micromol/L) were inhibited to secrete LTB4 dose-dependently, following the markedly down-regulated expressions of TNF-alpha (15%-66%) and IL-1beta (41%-71%) at mRNA level . MK-886 42-48 interleukin 1 beta Homo sapiens 233-241 16817014-4 2006 MK886, a 5-lipoxygenase activating protein (FLAP) inhibitor, induces apoptosis in many cell lines by an unknown mechanism that is independent of FLAP and lipoxygenase activity but is possibly related to effects on kinases such as Akt. MK-886 0-5 arachidonate 5-lipoxygenase activating protein Homo sapiens 44-48 16856209-7 2006 Administration of MIP-2 promoted a dose-dependent neutrophil migration in naive mice which was inhibited by repertaxin, anti-TNF-alpha, anti-MIP-1alpha antibodies or by MK886 (leukotriene synthesis inhibitor). MK-886 169-174 chemokine (C-X-C motif) ligand 2 Mus musculus 18-23 16545574-0 2006 Pre-treatment of HT-29 cells with 5-LOX inhibitor (MK-886) induces changes in cell cycle and increases apoptosis after photodynamic therapy with hypericin. MK-886 51-57 arachidonate 5-lipoxygenase Homo sapiens 34-39 16817014-4 2006 MK886, a 5-lipoxygenase activating protein (FLAP) inhibitor, induces apoptosis in many cell lines by an unknown mechanism that is independent of FLAP and lipoxygenase activity but is possibly related to effects on kinases such as Akt. MK-886 0-5 arachidonate 5-lipoxygenase activating protein Homo sapiens 145-149 16817014-4 2006 MK886, a 5-lipoxygenase activating protein (FLAP) inhibitor, induces apoptosis in many cell lines by an unknown mechanism that is independent of FLAP and lipoxygenase activity but is possibly related to effects on kinases such as Akt. MK-886 0-5 AKT serine/threonine kinase 1 Homo sapiens 230-233 16817014-6 2006 Following NAC-MK886 treatment, there was a significant increase in caspase-3 activity, and a decrease in mitochondrial transmembrane potential compared to MK886 alone. MK-886 14-19 caspase 3 Homo sapiens 67-76 16525884-6 2006 The inhibition of LPS- and TNF-alpha-induced NF-kappaB luciferase activity in macrophages was abolished by MK-886, a selective PPAR-alpha antagonist. MK-886 107-113 peroxisome proliferator activated receptor alpha Homo sapiens 127-137 16551867-1 2006 The small molecular inhibitor MK886 is known to block 5-lipoxygenase-activating protein ALOX5AP and shows antitumor activity in multiple human cell lines. MK-886 30-35 arachidonate 5-lipoxygenase Homo sapiens 54-68 16039040-1 2006 We investigated the role of the 5-lipoxygenase (5-LOX) pathway of arachidonic acid metabolism in tumour necrosis factor-alpha (TNF-alpha)-induced differentiation of human leukemic HL-60 cells using MK-886, an inhibitor of 5-LOX activating protein. MK-886 198-204 tumor necrosis factor Homo sapiens 127-136 16606359-8 2006 NMDA receptor antagonist MK-801 inhibited almost all the responses to OGD and NMDA; whereas 5-LOX activating protein inhibitor MK-886 and 5-LOX inhibitor caffeic acid inhibited the reduction of neuron viability and the production of CysLTs, but did not affect 5-LOX translocation. MK-886 127-133 lysyl oxidase Rattus norvegicus 94-97 16547963-9 2006 In conclusion, intrapulmonary application of the 5-lipoxygenase inhibitor MK886 with surfactant as a carrier improves lung function by decreasing EVLW as the main response to LTB(4) reduction. MK-886 74-79 arachidonate 5-lipoxygenase Homo sapiens 49-63 16039040-2 2006 MK-886 augmented cell cycle arrest and differentiation induced by TNF-alpha; however, both effects were probably 5-LOX-independent, because a general LOX inhibitor, NDGA, had no effect. MK-886 0-6 tumor necrosis factor Homo sapiens 66-75 16039040-3 2006 Apoptosis was significantly elevated after combined TNF-alpha and MK-886 treatment, which could be partially associated with changes of Mcl-1 protein expression. MK-886 66-72 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 136-141 16039040-5 2006 Thus, in addition to apoptosis, MK-886 can enhance TNF-alpha-induced differentiation. MK-886 32-38 tumor necrosis factor Homo sapiens 51-60 16551867-1 2006 The small molecular inhibitor MK886 is known to block 5-lipoxygenase-activating protein ALOX5AP and shows antitumor activity in multiple human cell lines. MK-886 30-35 arachidonate 5-lipoxygenase activating protein Homo sapiens 88-95 15953724-0 2005 Inhibitors of the inducible microsomal prostaglandin E2 synthase (mPGES-1) derived from MK-886. MK-886 88-94 prostaglandin E synthase Mus musculus 66-73 16148135-9 2005 In the lung parenchyma of infected animals, MK886 significantly inhibited synthesis of IL-5 at the beginning of infection, whereas levels of IL-12 increased progressively throughout the postinfection period. MK-886 44-49 interleukin 5 Mus musculus 87-91 16148135-11 2005 Nevertheless, IgE and IgG1 (but not IgG2a) synthesis was also significantly inhibited by MK886 administration. MK-886 89-94 LOC105243590 Mus musculus 22-26 16506957-0 2006 Inhibition of five lipoxygenase activating protein (FLAP) by MK-886 decreases atherosclerosis in apoE/LDLR-double knockout mice. MK-886 61-67 arachidonate 5-lipoxygenase activating protein Mus musculus 52-56 16506957-0 2006 Inhibition of five lipoxygenase activating protein (FLAP) by MK-886 decreases atherosclerosis in apoE/LDLR-double knockout mice. MK-886 61-67 apolipoprotein E Mus musculus 97-101 16506957-0 2006 Inhibition of five lipoxygenase activating protein (FLAP) by MK-886 decreases atherosclerosis in apoE/LDLR-double knockout mice. MK-886 61-67 low density lipoprotein receptor Mus musculus 102-106 16506957-3 2006 We hypothesized that MK-886, an inhibitor of FLAP, could attenuate the development of atherosclerosis in the atherogenic apolipoprotein E/low density lipoprotein receptor (apoE/LDLR) double knockout (DKO) mouse model. MK-886 21-27 arachidonate 5-lipoxygenase activating protein Mus musculus 45-49 16506957-3 2006 We hypothesized that MK-886, an inhibitor of FLAP, could attenuate the development of atherosclerosis in the atherogenic apolipoprotein E/low density lipoprotein receptor (apoE/LDLR) double knockout (DKO) mouse model. MK-886 21-27 apolipoprotein E Mus musculus 172-176 16506957-3 2006 We hypothesized that MK-886, an inhibitor of FLAP, could attenuate the development of atherosclerosis in the atherogenic apolipoprotein E/low density lipoprotein receptor (apoE/LDLR) double knockout (DKO) mouse model. MK-886 21-27 low density lipoprotein receptor Mus musculus 177-181 16506957-11 2006 CONCLUSIONS: Our results show for the first time that inhibition of FLAP by MK-886 reduces development of atherosclerosis in gene-targeted apoE/LDLR-DKO mice. MK-886 76-82 arachidonate 5-lipoxygenase activating protein Mus musculus 68-72 16506957-11 2006 CONCLUSIONS: Our results show for the first time that inhibition of FLAP by MK-886 reduces development of atherosclerosis in gene-targeted apoE/LDLR-DKO mice. MK-886 76-82 apolipoprotein E Mus musculus 139-143 16506957-11 2006 CONCLUSIONS: Our results show for the first time that inhibition of FLAP by MK-886 reduces development of atherosclerosis in gene-targeted apoE/LDLR-DKO mice. MK-886 76-82 low density lipoprotein receptor Mus musculus 144-148 16374165-8 2006 All events were abolished when formation of cysteinyl-leukotrienes was blocked by the 5-lipoxygenase activity inhibitor MK-886, targeting 5-lipoxygenase activating protein. MK-886 120-126 arachidonate 5-lipoxygenase Rattus norvegicus 86-100 16374165-8 2006 All events were abolished when formation of cysteinyl-leukotrienes was blocked by the 5-lipoxygenase activity inhibitor MK-886, targeting 5-lipoxygenase activating protein. MK-886 120-126 arachidonate 5-lipoxygenase Rattus norvegicus 138-152 16313356-6 2005 Pre-treatment with transforming growth factor-beta1 enhanced both stimulated leukotriene synthesis and the inhibitory effect of U-75302 and MK886 on IL-10 release from DCs. MK-886 140-145 interleukin 10 Mus musculus 149-154 16060857-6 2005 A similar induction of NGAL mRNA was observed in human breast cancer MCF7 cells treated with MK886, indicating this was not a cell-specific effect. MK-886 93-98 lipocalin 2 Homo sapiens 23-27 15953724-1 2005 A series of potent and selective inhibitors of the inducible microsomal PGE2 synthase (mPGES-1) has been developed based on the indole FLAP inhibitor MK-886. MK-886 150-156 prostaglandin E synthase Mus musculus 87-94 15953724-1 2005 A series of potent and selective inhibitors of the inducible microsomal PGE2 synthase (mPGES-1) has been developed based on the indole FLAP inhibitor MK-886. MK-886 150-156 arachidonate 5-lipoxygenase activating protein Homo sapiens 135-139 16164825-10 2005 The astrocyte P2X7- evoked rise of CysLT efflux was abolished in the presence of MK-886, an inhibitor of 5-lipoxygenase activating protein (FLAP) whose expression, along with that of 5-lipoxygenase (5-LO) was reported by Northern Blot analysis. MK-886 81-87 arachidonate 5-lipoxygenase Rattus norvegicus 105-119 15880139-8 2005 PGF extract and its component oleanolic acid enhanced PPAR-alpha luciferase reporter gene activity in human embryonic kidney 293 cells, and this effect was completely suppressed by a selective PPAR-alpha antagonist MK-886, consistent with the presence of PPAR-alpha activator activity in the extract and this component. MK-886 215-221 peroxisome proliferator activated receptor alpha Homo sapiens 54-64 15880139-8 2005 PGF extract and its component oleanolic acid enhanced PPAR-alpha luciferase reporter gene activity in human embryonic kidney 293 cells, and this effect was completely suppressed by a selective PPAR-alpha antagonist MK-886, consistent with the presence of PPAR-alpha activator activity in the extract and this component. MK-886 215-221 peroxisome proliferator activated receptor alpha Homo sapiens 193-203 15880139-8 2005 PGF extract and its component oleanolic acid enhanced PPAR-alpha luciferase reporter gene activity in human embryonic kidney 293 cells, and this effect was completely suppressed by a selective PPAR-alpha antagonist MK-886, consistent with the presence of PPAR-alpha activator activity in the extract and this component. MK-886 215-221 peroxisome proliferator activated receptor alpha Homo sapiens 193-203 15779087-4 2005 In addition, the inhibition of LO by nordihydroguaiaretic acid (NDGA; general LO inhibitor) or MK886 (5-LO inhibitor), but not baicalein (12-LO inhibitor), completely abrogated the LPS-induced iNOS expression. MK-886 95-100 nitric oxide synthase 2 Homo sapiens 193-197 16164825-10 2005 The astrocyte P2X7- evoked rise of CysLT efflux was abolished in the presence of MK-886, an inhibitor of 5-lipoxygenase activating protein (FLAP) whose expression, along with that of 5-lipoxygenase (5-LO) was reported by Northern Blot analysis. MK-886 81-87 arachidonate 5-lipoxygenase activating protein Rattus norvegicus 140-144 16164825-10 2005 The astrocyte P2X7- evoked rise of CysLT efflux was abolished in the presence of MK-886, an inhibitor of 5-lipoxygenase activating protein (FLAP) whose expression, along with that of 5-lipoxygenase (5-LO) was reported by Northern Blot analysis. MK-886 81-87 arachidonate 5-lipoxygenase Rattus norvegicus 183-197 15070903-5 2004 The number of cells killed by A23187 was doubled by treatment with 0.5 microm MK886 and 5 microm indomethacin, which inhibit arachidonic acid metabolism through the 5-lipoxygenase and cyclooxygenase pathway, respectively. MK-886 78-83 arachidonate 5-lipoxygenase Rattus norvegicus 165-179 15899809-2 2005 We have previously reported that exposure to the 5-lipoxygenase activating protein-directed inhibitor MK886 but not the cyclooxygenase inhibitor, indomethacin, reduced growth, increased apoptosis, and up-regulated PPARalpha and gamma expression in breast cancer cell lines. MK-886 102-107 arachidonate 5-lipoxygenase Homo sapiens 49-63 15899809-2 2005 We have previously reported that exposure to the 5-lipoxygenase activating protein-directed inhibitor MK886 but not the cyclooxygenase inhibitor, indomethacin, reduced growth, increased apoptosis, and up-regulated PPARalpha and gamma expression in breast cancer cell lines. MK-886 102-107 peroxisome proliferator activated receptor alpha Homo sapiens 214-223 15899809-4 2005 Non-small-cell cancer cell line A549 revealed dose-dependent PPARgamma reporter activity after treatment with MK886. MK-886 110-115 peroxisome proliferator activated receptor gamma Homo sapiens 61-70 15899809-6 2005 We also show increased growth inhibition and up-regulation of apoptosis after exposure to MK886 alone, or in combination with indomethacin and the PPAR ligand, 15-deoxy-Delta12,14-prostaglandin J2 compared with single drug exposures on the adenocarcinoma cell line A549 and small-cell cancer cell lines H345, N417, and H510. MK-886 90-95 peroxisome proliferator activated receptor alpha Homo sapiens 147-151 15899809-7 2005 Real-time PCR analyses showed increased PPAR mRNA and retinoid X receptor (RXR)alpha mRNA expression after exposure to MK886 and indomethacin in a time-dependent fashion. MK-886 119-124 peroxisome proliferator activated receptor alpha Homo sapiens 40-44 15899809-7 2005 Real-time PCR analyses showed increased PPAR mRNA and retinoid X receptor (RXR)alpha mRNA expression after exposure to MK886 and indomethacin in a time-dependent fashion. MK-886 119-124 retinoid X receptor alpha Homo sapiens 54-73 15454480-5 2005 At a concentration of 100 nM, the drugs BWA4C (a specific 5-lipoxygenase inhibitor) and MK-886 (a specific 5-lipoxygenase activating protein inhibitor) markedly inhibited CD40-induced DNA synthesis (45% and 38%, respectively) and CD40-induced expression of CD23, CD54, and CD150. MK-886 88-94 arachidonate 5-lipoxygenase Homo sapiens 107-121 15454480-5 2005 At a concentration of 100 nM, the drugs BWA4C (a specific 5-lipoxygenase inhibitor) and MK-886 (a specific 5-lipoxygenase activating protein inhibitor) markedly inhibited CD40-induced DNA synthesis (45% and 38%, respectively) and CD40-induced expression of CD23, CD54, and CD150. MK-886 88-94 CD40 molecule Homo sapiens 171-175 15454480-5 2005 At a concentration of 100 nM, the drugs BWA4C (a specific 5-lipoxygenase inhibitor) and MK-886 (a specific 5-lipoxygenase activating protein inhibitor) markedly inhibited CD40-induced DNA synthesis (45% and 38%, respectively) and CD40-induced expression of CD23, CD54, and CD150. MK-886 88-94 CD40 molecule Homo sapiens 230-234 15454480-5 2005 At a concentration of 100 nM, the drugs BWA4C (a specific 5-lipoxygenase inhibitor) and MK-886 (a specific 5-lipoxygenase activating protein inhibitor) markedly inhibited CD40-induced DNA synthesis (45% and 38%, respectively) and CD40-induced expression of CD23, CD54, and CD150. MK-886 88-94 Fc epsilon receptor II Homo sapiens 257-261 15454480-5 2005 At a concentration of 100 nM, the drugs BWA4C (a specific 5-lipoxygenase inhibitor) and MK-886 (a specific 5-lipoxygenase activating protein inhibitor) markedly inhibited CD40-induced DNA synthesis (45% and 38%, respectively) and CD40-induced expression of CD23, CD54, and CD150. MK-886 88-94 intercellular adhesion molecule 1 Homo sapiens 263-267 15454480-5 2005 At a concentration of 100 nM, the drugs BWA4C (a specific 5-lipoxygenase inhibitor) and MK-886 (a specific 5-lipoxygenase activating protein inhibitor) markedly inhibited CD40-induced DNA synthesis (45% and 38%, respectively) and CD40-induced expression of CD23, CD54, and CD150. MK-886 88-94 signaling lymphocytic activation molecule family member 1 Homo sapiens 273-278 15630695-5 2005 The ability of iPLA2 inhibitors to increase GluR1 phosphorylation was mimicked by the 5-lipoxygenase (5-LO) inhibitor MK-886, but not by blockers of 12-lipoxygenase (12-LO) or cyclooxygenase. MK-886 118-124 phospholipase A2 group VI Homo sapiens 15-20 15630695-5 2005 The ability of iPLA2 inhibitors to increase GluR1 phosphorylation was mimicked by the 5-lipoxygenase (5-LO) inhibitor MK-886, but not by blockers of 12-lipoxygenase (12-LO) or cyclooxygenase. MK-886 118-124 glutamate ionotropic receptor AMPA type subunit 1 Homo sapiens 44-49 15630695-5 2005 The ability of iPLA2 inhibitors to increase GluR1 phosphorylation was mimicked by the 5-lipoxygenase (5-LO) inhibitor MK-886, but not by blockers of 12-lipoxygenase (12-LO) or cyclooxygenase. MK-886 118-124 arachidonate 5-lipoxygenase Homo sapiens 86-100 15517864-1 2004 BACKGROUND: MK 886, a 5-lipoxygenase inhibitor, induces a type 1 "apoptotic" form of programmed cell death in Bcl-2-positive U937 monoblastoid cells. MK-886 12-18 arachidonate 5-lipoxygenase Homo sapiens 22-36 15517864-1 2004 BACKGROUND: MK 886, a 5-lipoxygenase inhibitor, induces a type 1 "apoptotic" form of programmed cell death in Bcl-2-positive U937 monoblastoid cells. MK-886 12-18 BCL2 apoptosis regulator Homo sapiens 110-115 15517864-7 2004 Two chemicals that inhibit the function of Bcl-2, HA14-1 and 2-methyl-antimycin A3, reduced the Ca2+ response to MK 886, if pre-incubated with the Bcl-2-positive U937 cells at 37 degrees C for several hours. MK-886 113-119 BCL2 apoptosis regulator Homo sapiens 43-48 15517864-7 2004 Two chemicals that inhibit the function of Bcl-2, HA14-1 and 2-methyl-antimycin A3, reduced the Ca2+ response to MK 886, if pre-incubated with the Bcl-2-positive U937 cells at 37 degrees C for several hours. MK-886 113-119 BCL2 apoptosis regulator Homo sapiens 147-152 15517864-8 2004 MK 886 was previously shown to induce reactive oxygen species and a fall in mitochondrial membrane potential in both Bcl-2-positive U937 and in Bcl-2-negative PC-3 prostate and panc-1 pancreatic cancer cells. MK-886 0-6 BCL2 apoptosis regulator Homo sapiens 117-122 15517864-8 2004 MK 886 was previously shown to induce reactive oxygen species and a fall in mitochondrial membrane potential in both Bcl-2-positive U937 and in Bcl-2-negative PC-3 prostate and panc-1 pancreatic cancer cells. MK-886 0-6 BCL2 apoptosis regulator Homo sapiens 144-149 15899809-7 2005 Real-time PCR analyses showed increased PPAR mRNA and retinoid X receptor (RXR)alpha mRNA expression after exposure to MK886 and indomethacin in a time-dependent fashion. MK-886 119-124 retinoid X receptor alpha Homo sapiens 75-84 15899809-10 2005 The combination of low-dose MK886, ciglitazone, and 13-cis-retinoic acid interacted at least in a superadditive fashion to inhibit the growth of lung cancer cell lines A549 and H1299, suggesting that targeting PPARgamma and AA action is a promising approach to lung cancer growth with a favorable therapeutic index. MK-886 28-33 peroxisome proliferator activated receptor gamma Homo sapiens 210-219 15458923-7 2005 However, MK-886 did inhibit IL-1beta-stimulated PGES activity in vitro by 86.8%. MK-886 9-15 interleukin 1 beta Homo sapiens 28-36 15458923-7 2005 However, MK-886 did inhibit IL-1beta-stimulated PGES activity in vitro by 86.8%. MK-886 9-15 prostaglandin E synthase Homo sapiens 48-52 15458923-9 2005 In contrast, NS-398 did not inhibit VEGF production at 8 h, and only partially at 24 h, whereas MK-886 totally inhibited VEGF production at each time point. MK-886 96-102 vascular endothelial growth factor A Homo sapiens 121-125 15796162-1 2005 Micromolar concentrations of the five-lipoxygenase inhibitor, MK 886 induce a "type 1" (apoptotic, extrinsic, death domain, receptor-dependent, caspase-positive) form of programmed cell death in Bcl-2-positive U937 human monoblastoid and HL-60 myeloid leukemia cells. MK-886 62-68 BCL2 apoptosis regulator Homo sapiens 195-200 15796162-7 2005 Bcl-2-positive HeLa cervical cancer cells exhibited an acute MK 886-induced increase in Ca2+. MK-886 61-67 BCL2 apoptosis regulator Homo sapiens 0-5 15607561-0 2005 Disparate forms of MK 886-induced programmed death in BCL-2 (+) blood and BCL-2 (-) solid cancer cells and a putative "nuclear" Ca2+ channel: "soil" trumps "seed"? MK-886 19-25 BCL2 apoptosis regulator Homo sapiens 54-59 15607561-0 2005 Disparate forms of MK 886-induced programmed death in BCL-2 (+) blood and BCL-2 (-) solid cancer cells and a putative "nuclear" Ca2+ channel: "soil" trumps "seed"? MK-886 19-25 BCL2 apoptosis regulator Homo sapiens 74-79 15607561-1 2005 UNLABELLED: The five-lipoxygenase inhibitor, MK 886, in micromolar concentration induces a "type 1" form of programmed cell death in U937 human monoblastoid cells and a "type 2" form in Panc-1 pancreatic and PC3 prostate cell lines. MK-886 45-51 proprotein convertase subtilisin/kexin type 1 Homo sapiens 208-211 15607561-5 2005 Solid tumor-derived Bcl-2-positive HeLa cervical cancer cells exhibit an acute increase in Ca(2+) after challenge with MK 886. MK-886 119-125 BCL2 apoptosis regulator Homo sapiens 20-25 15132836-5 2004 RESULTS: 5-Lipoxygenase inhibitors nordihydroguaiaretic acid, AA861 and MK886, could suppress the expression of ICAM-1 protein as well as of its mRNA in a375 cells and reduce the adhesion of a375 to EC304. MK-886 72-77 arachidonate 5-lipoxygenase Homo sapiens 9-23 15132836-5 2004 RESULTS: 5-Lipoxygenase inhibitors nordihydroguaiaretic acid, AA861 and MK886, could suppress the expression of ICAM-1 protein as well as of its mRNA in a375 cells and reduce the adhesion of a375 to EC304. MK-886 72-77 intercellular adhesion molecule 1 Homo sapiens 112-118 15225371-13 2004 Conversion of PGH2 to PGE2 (PGES activity) was significantly increased in the lysate from IL-1beta-stimulated chondrocytes and it was inhibited by MK-886, which has an inhibitory effect on mPGES-1 activity. MK-886 147-153 prostaglandin E synthase Homo sapiens 28-32 14656710-17 2004 MK886, a selective 5-lipoxygenase inhibitor, inhibited OxAA stimulation of LTB(4) and IL-8 also in a dose-response manner. MK-886 0-5 arachidonate 5-lipoxygenase Homo sapiens 19-33 14656710-17 2004 MK886, a selective 5-lipoxygenase inhibitor, inhibited OxAA stimulation of LTB(4) and IL-8 also in a dose-response manner. MK-886 0-5 C-X-C motif chemokine ligand 8 Homo sapiens 86-90 15225371-13 2004 Conversion of PGH2 to PGE2 (PGES activity) was significantly increased in the lysate from IL-1beta-stimulated chondrocytes and it was inhibited by MK-886, which has an inhibitory effect on mPGES-1 activity. MK-886 147-153 interleukin 1 beta Homo sapiens 90-98 15225371-13 2004 Conversion of PGH2 to PGE2 (PGES activity) was significantly increased in the lysate from IL-1beta-stimulated chondrocytes and it was inhibited by MK-886, which has an inhibitory effect on mPGES-1 activity. MK-886 147-153 prostaglandin E synthase Mus musculus 189-196 12895593-3 2003 The enzymatic activity of LTC(4) synthase is augmented by Mg(2+) and inhibited by Co(2+) and the FLAP inhibitor MK-886. MK-886 112-118 leukotriene C4 synthase Homo sapiens 26-41 14675240-0 2004 Five-lipoxygenase-activating protein inhibitor MK-886 induces apoptosis in gastric cancer through upregulation of p27kip1 and bax. MK-886 47-53 cyclin dependent kinase inhibitor 1B Homo sapiens 114-121 14675240-0 2004 Five-lipoxygenase-activating protein inhibitor MK-886 induces apoptosis in gastric cancer through upregulation of p27kip1 and bax. MK-886 47-53 BCL2 associated X, apoptosis regulator Homo sapiens 126-129 14675240-3 2004 Here, the authors investigated the effect of a FLAP inhibitor, MK-886, on the inhibition of proliferation and induction of apoptosis in gastric cancer. MK-886 63-69 arachidonate 5-lipoxygenase activating protein Homo sapiens 47-51 14675240-10 2004 Specific caspase-3 inhibitors partially blocked MK-886-induced apoptosis. MK-886 48-54 caspase 3 Homo sapiens 9-18 14675240-11 2004 CONCLUSION: The present results suggest that MK-886 induces apoptosis in gastric cancer cells through upregulation of p27kip1 and bax, and that MK-886 is a potentially useful drug in gastric cancer prevention and therapy. MK-886 45-51 cyclin dependent kinase inhibitor 1B Homo sapiens 118-125 14675240-11 2004 CONCLUSION: The present results suggest that MK-886 induces apoptosis in gastric cancer cells through upregulation of p27kip1 and bax, and that MK-886 is a potentially useful drug in gastric cancer prevention and therapy. MK-886 45-51 BCL2 associated X, apoptosis regulator Homo sapiens 130-133 14675240-11 2004 CONCLUSION: The present results suggest that MK-886 induces apoptosis in gastric cancer cells through upregulation of p27kip1 and bax, and that MK-886 is a potentially useful drug in gastric cancer prevention and therapy. MK-886 144-150 cyclin dependent kinase inhibitor 1B Homo sapiens 118-125 14675240-11 2004 CONCLUSION: The present results suggest that MK-886 induces apoptosis in gastric cancer cells through upregulation of p27kip1 and bax, and that MK-886 is a potentially useful drug in gastric cancer prevention and therapy. MK-886 144-150 BCL2 associated X, apoptosis regulator Homo sapiens 130-133 12882972-4 2003 This IkappaBalpha-induced apoA-I increase was blocked by preincubation with MK886, a selective inhibitor of peroxisome proliferator-activated receptor alpha (PPARalpha), suggesting that NFkappaB inactivation induces apoA-I through activation of PPARalpha. MK-886 76-81 NFKB inhibitor alpha Homo sapiens 5-17 12882972-4 2003 This IkappaBalpha-induced apoA-I increase was blocked by preincubation with MK886, a selective inhibitor of peroxisome proliferator-activated receptor alpha (PPARalpha), suggesting that NFkappaB inactivation induces apoA-I through activation of PPARalpha. MK-886 76-81 apolipoprotein A1 Homo sapiens 26-32 12882972-4 2003 This IkappaBalpha-induced apoA-I increase was blocked by preincubation with MK886, a selective inhibitor of peroxisome proliferator-activated receptor alpha (PPARalpha), suggesting that NFkappaB inactivation induces apoA-I through activation of PPARalpha. MK-886 76-81 peroxisome proliferator activated receptor alpha Homo sapiens 108-156 12882972-4 2003 This IkappaBalpha-induced apoA-I increase was blocked by preincubation with MK886, a selective inhibitor of peroxisome proliferator-activated receptor alpha (PPARalpha), suggesting that NFkappaB inactivation induces apoA-I through activation of PPARalpha. MK-886 76-81 peroxisome proliferator activated receptor alpha Homo sapiens 158-167 12882972-4 2003 This IkappaBalpha-induced apoA-I increase was blocked by preincubation with MK886, a selective inhibitor of peroxisome proliferator-activated receptor alpha (PPARalpha), suggesting that NFkappaB inactivation induces apoA-I through activation of PPARalpha. MK-886 76-81 nuclear factor kappa B subunit 1 Homo sapiens 186-194 12882972-4 2003 This IkappaBalpha-induced apoA-I increase was blocked by preincubation with MK886, a selective inhibitor of peroxisome proliferator-activated receptor alpha (PPARalpha), suggesting that NFkappaB inactivation induces apoA-I through activation of PPARalpha. MK-886 76-81 apolipoprotein A1 Homo sapiens 216-222 12882972-4 2003 This IkappaBalpha-induced apoA-I increase was blocked by preincubation with MK886, a selective inhibitor of peroxisome proliferator-activated receptor alpha (PPARalpha), suggesting that NFkappaB inactivation induces apoA-I through activation of PPARalpha. MK-886 76-81 peroxisome proliferator activated receptor alpha Homo sapiens 245-254 12882972-5 2003 To further support this idea, the expression of IkappaBalpha increased apoA-I promoter activity, and this increase was blocked by preincubation with MK886. MK-886 149-154 NFKB inhibitor alpha Homo sapiens 48-60 12882972-5 2003 To further support this idea, the expression of IkappaBalpha increased apoA-I promoter activity, and this increase was blocked by preincubation with MK886. MK-886 149-154 apolipoprotein A1 Homo sapiens 71-77 12914802-7 2003 Blockade of 5-LOX by MK886 (200nM) abrogated LTB(4)-formation, ROS-formation, and IL-6 mRNA expression. MK-886 21-26 arachidonate 5-lipoxygenase Rattus norvegicus 14-17 12914802-7 2003 Blockade of 5-LOX by MK886 (200nM) abrogated LTB(4)-formation, ROS-formation, and IL-6 mRNA expression. MK-886 21-26 interleukin 6 Rattus norvegicus 82-86 12782627-6 2003 The effect of exogenous sPLA2s is also blocked by the PPAR alpha inhibitor MK886. MK-886 75-80 phospholipase A2 group IID Homo sapiens 24-30 12782627-6 2003 The effect of exogenous sPLA2s is also blocked by the PPAR alpha inhibitor MK886. MK-886 75-80 peroxisome proliferator activated receptor alpha Homo sapiens 54-64 12782627-7 2003 Interestingly, the expression of sPLA2-IIA induced by TNF alpha alone is also attenuated by MK886, by the sPLA2-IIA inhibitor LY311727, by heparinase, which prevents the binding of sPLA2-IIA to heparan sulfate proteoglycans, and by the specific cPLA2-alpha inhibitor pyrrolidine-1. MK-886 92-97 phospholipase A2 group IIA Homo sapiens 33-38 12782627-7 2003 Interestingly, the expression of sPLA2-IIA induced by TNF alpha alone is also attenuated by MK886, by the sPLA2-IIA inhibitor LY311727, by heparinase, which prevents the binding of sPLA2-IIA to heparan sulfate proteoglycans, and by the specific cPLA2-alpha inhibitor pyrrolidine-1. MK-886 92-97 tumor necrosis factor Homo sapiens 54-63 12782627-7 2003 Interestingly, the expression of sPLA2-IIA induced by TNF alpha alone is also attenuated by MK886, by the sPLA2-IIA inhibitor LY311727, by heparinase, which prevents the binding of sPLA2-IIA to heparan sulfate proteoglycans, and by the specific cPLA2-alpha inhibitor pyrrolidine-1. MK-886 92-97 phospholipase A2 group IVA Homo sapiens 245-256 12895593-3 2003 The enzymatic activity of LTC(4) synthase is augmented by Mg(2+) and inhibited by Co(2+) and the FLAP inhibitor MK-886. MK-886 112-118 arachidonate 5-lipoxygenase activating protein Homo sapiens 97-101 12614196-1 2003 MK886, a strong proapoptotic agent, is an inhibitor of 5-lipoxygenase (LOX) through binding to the 5-LOX-activating protein (FLAP). MK-886 0-5 arachidonate 5-lipoxygenase Mus musculus 55-69 12945742-2 2003 However, on the basis of the induction of apoptosis by the FLAP inhibitor MK886 in cells lacking 5-LOX, it is possible that this fatty acid-binding protein has other activities. MK-886 74-79 arachidonate 5-lipoxygenase activating protein Mus musculus 59-63 12614196-1 2003 MK886, a strong proapoptotic agent, is an inhibitor of 5-lipoxygenase (LOX) through binding to the 5-LOX-activating protein (FLAP). MK-886 0-5 arachidonate 5-lipoxygenase Mus musculus 71-74 12614196-10 2003 In all cases, including the inhibition of MK886-induced 24p3 protein expression by stable transfection with antisense cDNA of 24p3, the extent of apoptosis closely paralleled 24p3 levels. MK-886 42-47 solute carrier family 10 (sodium/bile acid cotransporter family), member 3 Mus musculus 58-68 12614196-1 2003 MK886, a strong proapoptotic agent, is an inhibitor of 5-lipoxygenase (LOX) through binding to the 5-LOX-activating protein (FLAP). MK-886 0-5 arachidonate 5-lipoxygenase Mus musculus 101-104 12614196-11 2003 Apoptosis induced by MK886, or enhanced by WY14643, was accompanied by the cleavage and activation of caspase-3. MK-886 21-26 caspase 3 Mus musculus 102-111 12614196-7 2003 The up-regulated 24p3 mRNA expression by MK886 was enhanced a further 3.1-fold by WY14643, an activator of peroxisome-proliferator-activated receptor alpha, whereas ciglitazone, an activator of peroxisome-proliferator-activated receptor gamma attenuated the MK886-induced 24p3 expression by more than 50%. MK-886 41-46 peroxisome proliferator activated receptor alpha Mus musculus 107-155 12614196-12 2003 The overexpression of bcl-2 or bcl-x(L) in FL5.12 cells inhibited apoptosis induced by MK886 as well as the enhancement of apoptosis by WY14643. MK-886 87-92 B cell leukemia/lymphoma 2 Mus musculus 22-27 12614196-7 2003 The up-regulated 24p3 mRNA expression by MK886 was enhanced a further 3.1-fold by WY14643, an activator of peroxisome-proliferator-activated receptor alpha, whereas ciglitazone, an activator of peroxisome-proliferator-activated receptor gamma attenuated the MK886-induced 24p3 expression by more than 50%. MK-886 41-46 peroxisome proliferator activated receptor gamma Mus musculus 194-242 12614196-12 2003 The overexpression of bcl-2 or bcl-x(L) in FL5.12 cells inhibited apoptosis induced by MK886 as well as the enhancement of apoptosis by WY14643. MK-886 87-92 BCL2-like 1 Mus musculus 31-36 12660222-3 2003 5-LOX inhibitors, 5,8,11,14-eicosatetraynoic acid and caffeic acid, completely prevented apoptosis, whereas the phospholipase A(2) inhibitor methyl-arachidonoyl fluorophosphonate and the 5-LOX activating protein inhibitor MK886 reduced it to 65-70%. MK-886 222-227 arachidonate 5-lipoxygenase Homo sapiens 0-5 12565196-1 2003 MK886, an inhibitor of 5-lipoxygenase activating protein (FLAP), and the lipoxygenase (LOX) inhibitors baicalein and nordihydroguaiaretic acid (NDGA), induce apoptosis by mechanisms independent of both LOX and FLAP. MK-886 0-5 arachidonate 5-lipoxygenase activating protein Mus musculus 210-214 12565196-4 2003 MK886, baicalein, and NDGA significantly enhanced the release of [3H]-AA two to threefold within 2 h and induced apoptosis by 8 h. Neither MK886-induced AA release, nor apoptosis were affected by quinacrine, a phospholipase A2 inhibitor. MK-886 0-5 phospholipase A2, group IB, pancreas Mus musculus 210-226 11389700-14 2001 This is consistent with MK886 functioning as a non-competitive inhibitor of PPAR alpha, but may also indicate that PPAR alpha is not directly involved in MK886-induced apoptosis. MK-886 24-29 peroxisome proliferator activated receptor alpha Homo sapiens 76-80 12432940-3 2002 The enzyme activity of LTC4S is augmented by Mg2+ and inhibited by Co2+ and the function of 5-lipoxygenase (LO) activating protein (FLAP) inhibitor MK-886. MK-886 148-154 leukotriene C4 synthase Mus musculus 23-28 12432940-3 2002 The enzyme activity of LTC4S is augmented by Mg2+ and inhibited by Co2+ and the function of 5-lipoxygenase (LO) activating protein (FLAP) inhibitor MK-886. MK-886 148-154 arachidonate 5-lipoxygenase Mus musculus 92-106 12054916-0 2002 Increased cytosol Ca(2+) and type 1 programmed cell death in Bcl-2-positive U937 but not in Bcl-2-negative PC-3 and Panc-1 cells induced by the 5-lipoxygenase inhibitor MK 886. MK-886 169-175 arachidonate 5-lipoxygenase Homo sapiens 144-158 12054916-1 2002 MK 886, an arachidonic acid-related analog which inhibits the enzyme, 5-lipoxygenase by an indirect mechanism involving the 5-lipoxygenase activating protein, rapidly increased U937 cytosol Ca(2+), much of which localized around the cell nuclei. MK-886 0-6 arachidonate 5-lipoxygenase Homo sapiens 70-84 12054916-1 2002 MK 886, an arachidonic acid-related analog which inhibits the enzyme, 5-lipoxygenase by an indirect mechanism involving the 5-lipoxygenase activating protein, rapidly increased U937 cytosol Ca(2+), much of which localized around the cell nuclei. MK-886 0-6 arachidonate 5-lipoxygenase Homo sapiens 124-138 11877481-5 2002 Additionally, pretreatment of hMCs with MK571 or with the cys-LT biosynthetic inhibitor MK886 decreased IL-5 and TNF-alpha production in response to IgE receptor cross-linkage, implying a positive feedback by endogenously produced cys-LTs. MK-886 88-93 Miles-Carpenter X-linked mental retardation syndrome Homo sapiens 30-34 11877481-5 2002 Additionally, pretreatment of hMCs with MK571 or with the cys-LT biosynthetic inhibitor MK886 decreased IL-5 and TNF-alpha production in response to IgE receptor cross-linkage, implying a positive feedback by endogenously produced cys-LTs. MK-886 88-93 interleukin 5 Homo sapiens 104-108 11877481-5 2002 Additionally, pretreatment of hMCs with MK571 or with the cys-LT biosynthetic inhibitor MK886 decreased IL-5 and TNF-alpha production in response to IgE receptor cross-linkage, implying a positive feedback by endogenously produced cys-LTs. MK-886 88-93 tumor necrosis factor Homo sapiens 113-122 12033433-6 2002 Although the 5-LOX activating protein inhibitor MK886 killed these cells, another 5-LOX inhibitor AA861 hardly showed any effect. MK-886 48-53 arachidonate 5-lipoxygenase Homo sapiens 13-18 11748223-4 2002 The biosynthesis of FOG(7) in the macrophage was inhibited by MK-886, a known inhibitor of LTC(4) synthase, suggesting that this nuclear membrane-bound enzyme might be responsible for GSH conjugation to 5-oxoETE in the intact cell. MK-886 62-68 leukotriene C4 synthase Mus musculus 91-106 11739237-9 2001 Supernatant chemotactic activity is due to TNFalpha and LTB(4), since its release was inhibited by MK 886 (93%) and dexamethasone (90%), and significant amounts of these mediators were detected. MK-886 99-105 tumor necrosis factor Mus musculus 43-51 11389700-0 2001 Inhibition of peroxisome-proliferator-activated receptor (PPAR)alpha by MK886. MK-886 72-77 peroxisome proliferator activated receptor alpha Homo sapiens 58-62 11389700-6 2001 The ability of MK886 to inhibit PPAR-alpha, -beta and -gamma activity was assessed using reporter assay systems (peroxisome-proliferator response element--luciferase). MK-886 15-20 peroxisome proliferator activated receptor alpha Homo sapiens 32-36 11389700-7 2001 Using a transient transfection system in monkey kidney fibroblast CV-1 cells, mouse keratinocyte 308 cells and human lung adenocarcinoma A549 cells, 10--20 microM MK886 inhibited Wy14,643 activation of PPAR alpha by approximately 80%. MK-886 163-168 peroxisome proliferator activated receptor alpha Homo sapiens 202-212 11389700-8 2001 Similar inhibition of PPAR alpha by MK886 was observed with a stable transfection reporter system in CV-1 cells. MK-886 36-41 peroxisome proliferator activated receptor alpha Homo sapiens 22-26 11389700-10 2001 MK886 inhibited PPAR alpha by a non-competitive mechanism as shown by its effects on the binding of arachidonic acid to PPAR alpha protein, and a dose-response study using a transient transfection reporter assay in COS-1 cells. MK-886 0-5 peroxisome proliferator activated receptor alpha Homo sapiens 16-20 11389700-10 2001 MK886 inhibited PPAR alpha by a non-competitive mechanism as shown by its effects on the binding of arachidonic acid to PPAR alpha protein, and a dose-response study using a transient transfection reporter assay in COS-1 cells. MK-886 0-5 peroxisome proliferator activated receptor alpha Homo sapiens 120-124 11389700-11 2001 An assay assessing PPAR ligand-receptor interactions showed that MK886 prevents the conformational change necessary for active-complex formation. MK-886 65-70 peroxisome proliferator activated receptor alpha Homo sapiens 19-23 12475913-4 2003 Both MK-886, an antagonist of PPARalpha, and a dominant negative form of PPARalpha transfected into INS(832/13) cells caused a significant reduction in GIPR expression in low, but not high, glucose conditions. MK-886 5-11 peroxisome proliferator activated receptor alpha Rattus norvegicus 30-39 12475913-4 2003 Both MK-886, an antagonist of PPARalpha, and a dominant negative form of PPARalpha transfected into INS(832/13) cells caused a significant reduction in GIPR expression in low, but not high, glucose conditions. MK-886 5-11 gastric inhibitory polypeptide receptor Rattus norvegicus 152-156 12496393-4 2003 The same effect was observed with MK-886, a 5-LO-activating protein (FLAP)-specific inhibitor. MK-886 34-40 arachidonate 5-lipoxygenase activating protein Homo sapiens 69-73 12394960-11 2002 The employment of a platelet-activating factor receptor antagonist (WEB 2086) blocked leukotriene synthesis, and both WEB 2086 and a 5-lipoxygenase inhibitor (MK-886) suppressed the respiratory burst linked with this second priming pathway. MK-886 159-165 arachidonate 5-lipoxygenase Homo sapiens 133-147 12080072-6 2002 Treatment with 1 microM MK886 plus indomethacin sensitized cells to killing by exogenous arachidonic acid, which induces PTP opening and cytochrome c release (Scorrano, L., Penzo, D., Petronilli, V., Pagano, F., and Bernardi, P. (2001) J. Biol. MK-886 24-29 cytochrome c, somatic Homo sapiens 137-149 12054916-0 2002 Increased cytosol Ca(2+) and type 1 programmed cell death in Bcl-2-positive U937 but not in Bcl-2-negative PC-3 and Panc-1 cells induced by the 5-lipoxygenase inhibitor MK 886. MK-886 169-175 BCL2 apoptosis regulator Homo sapiens 61-66 11856764-5 2002 MK886, known as a noncompetitive inhibitor of PPAR(alpha), completely abolished the potentiation of sPLA(2)-IIA secretion and activity by WY14643, thus indicating that the effect of WY14643 is specifically mediated by PPAR(alpha). MK-886 0-5 peroxisome proliferator activated receptor alpha Rattus norvegicus 46-50 11856764-5 2002 MK886, known as a noncompetitive inhibitor of PPAR(alpha), completely abolished the potentiation of sPLA(2)-IIA secretion and activity by WY14643, thus indicating that the effect of WY14643 is specifically mediated by PPAR(alpha). MK-886 0-5 peroxisome proliferator activated receptor alpha Rattus norvegicus 218-222 11739237-11 2001 TNFalpha and LTB(4) released by OVA challenge seem to act through a sequential mechanism, since MK 886 inhibited (88%) neutrophil migration induced by TNFalpha. MK-886 96-102 tumor necrosis factor Mus musculus 0-8 11739237-11 2001 TNFalpha and LTB(4) released by OVA challenge seem to act through a sequential mechanism, since MK 886 inhibited (88%) neutrophil migration induced by TNFalpha. MK-886 96-102 tumor necrosis factor Mus musculus 151-159 11485388-0 2001 Proteolytic loss of bcl-x(L) in FL5.12 Cells undergoing apoptosis induced by MK886. MK-886 77-82 BCL2-like 1 Mus musculus 20-28 11485388-1 2001 Apoptosis induced in the IL3-dependent murine pro-B lymphocytic (FL5.12) cell line by the 5-lipoxygenase activating protein inhibitor MK886 is accompanied by the rapid loss of the anti-apoptotic bcl-x(L) and bcl-2, but not the proapoptotic bax proteins (Datta et al., J. Biol. MK-886 134-139 interleukin 3 Mus musculus 25-28 11485388-1 2001 Apoptosis induced in the IL3-dependent murine pro-B lymphocytic (FL5.12) cell line by the 5-lipoxygenase activating protein inhibitor MK886 is accompanied by the rapid loss of the anti-apoptotic bcl-x(L) and bcl-2, but not the proapoptotic bax proteins (Datta et al., J. Biol. MK-886 134-139 BCL2-like 1 Mus musculus 195-203 11485388-1 2001 Apoptosis induced in the IL3-dependent murine pro-B lymphocytic (FL5.12) cell line by the 5-lipoxygenase activating protein inhibitor MK886 is accompanied by the rapid loss of the anti-apoptotic bcl-x(L) and bcl-2, but not the proapoptotic bax proteins (Datta et al., J. Biol. MK-886 134-139 B cell leukemia/lymphoma 2 Mus musculus 208-213 11485388-6 2001 The disappearance of bcl-x(L) from FL5.12 cells upon MK886 treatment was prevented in a dose-dependent manner by pretreatment with leupeptin, pepstatin, phenylmethylsulfonyl fluoride, or the broad-spectrum caspase inhibitor Boc-D-FMK. MK-886 53-58 BCL2-like 1 Mus musculus 21-29 11485388-12 2001 This pathway may be unique to MK886 since these same protease inhibitors had only minimal effects on etoposide-induced apoptosis and the accompanying moderate loss of bcl-x(L) in FL5.12 cells. MK-886 30-35 BCL2-like 1 Mus musculus 167-175 11389700-15 2001 Although numerous PPAR activators have been identified, the results show that MK886 can inhibit PPAR alpha, making it the first compound identified to have such an effect. MK-886 78-83 peroxisome proliferator activated receptor alpha Homo sapiens 96-100 11350804-7 2001 The FLAP inhibitor MK-886, given to the animals before intratracheal SCF administration, significantly inhibited the release of LTC(4) and LTE(4) into the BAL fluid. MK-886 19-25 arachidonate 5-lipoxygenase activating protein Mus musculus 4-8 11350804-7 2001 The FLAP inhibitor MK-886, given to the animals before intratracheal SCF administration, significantly inhibited the release of LTC(4) and LTE(4) into the BAL fluid. MK-886 19-25 kit ligand Mus musculus 69-72 10913376-4 2000 MK-886, an inhibitor of 5-lipoxygenase is inefficient at blocking the vasoactive properties of cholesterol whereas NS-398, a selective inhibitor of cyclooxygenase-2 (COX-2) completely abolishes cholesterol-induced vasoconstriction. MK-886 0-6 arachidonate 5-lipoxygenase Rattus norvegicus 24-38 11311496-1 2001 The 5-lipoxygenase inhibitors SC41661A and MK886 with different mechanisms of action and the free radical spin trap, NTBN inhibit proliferation of the human bronchiolar lung cancer cell line NCI H-358 (5807 CRL). MK-886 43-48 arachidonate 5-lipoxygenase Homo sapiens 4-18 11333152-6 2001 In summary, the results indicate that during the application of MK-886 as a 5;-lipoxygenase inhibitor in neutrophils, the impact of the compound on the functional activity of the cells should be taken into consideration. MK-886 64-70 arachidonate 5-lipoxygenase Homo sapiens 76-91 11238189-8 2001 DNA synthesis of the cell line (Panc-1) with an activating point mutation in codon 12 of the ki-ras gene was significantly stimulated by NNK when cells were maintained in complete medium and this response was inhibited by the beta-blocker ICI118,551, the COX-inhibitor aspirin, or the 5-lipox-inhibitor MK-886. MK-886 303-309 KRAS proto-oncogene, GTPase Homo sapiens 93-99 11200053-5 2001 The CD69 expression induced by PAF and IL-5 on HES eosinophils and that by IL-5 on normal eosinophils were both inhibited by AA861 and MK-886, inhibitors of 5-LO activity. MK-886 135-141 CD69 molecule Homo sapiens 4-8 11200053-5 2001 The CD69 expression induced by PAF and IL-5 on HES eosinophils and that by IL-5 on normal eosinophils were both inhibited by AA861 and MK-886, inhibitors of 5-LO activity. MK-886 135-141 PCNA clamp associated factor Homo sapiens 31-34 11200053-5 2001 The CD69 expression induced by PAF and IL-5 on HES eosinophils and that by IL-5 on normal eosinophils were both inhibited by AA861 and MK-886, inhibitors of 5-LO activity. MK-886 135-141 interleukin 5 Homo sapiens 39-43 11200053-5 2001 The CD69 expression induced by PAF and IL-5 on HES eosinophils and that by IL-5 on normal eosinophils were both inhibited by AA861 and MK-886, inhibitors of 5-LO activity. MK-886 135-141 interleukin 5 Homo sapiens 75-79 11310854-4 2001 Activation of ERK was also effectively attenuated by the cyclooxygenase and lipoxygenase inhibitor BW755C and by the leukotriene biosynthesis inhibitor MK886, but the cyclooxygenase inhibitor indomethacin did not attenuate ERK activation. MK-886 152-157 Eph receptor B1 Rattus norvegicus 14-17 11238654-5 2001 These findings were related to an effect of mrp1 on LT metabolism, because survival was similar in mrp1(-/-) and wild-type mice treated with the 5-lipoxygenase-activating protein inhibitor MK-886. MK-886 189-195 ATP-binding cassette, sub-family B (MDR/TAP), member 1B Mus musculus 44-48 10913156-8 2000 Moreover, 5-lipoxygenase inhibitors 5,8,11,14-eicosatetraynoic acid and MK886, cyclooxygenase inhibitor indomethacin, caspase-3 and caspase-9 inhibitors Z-DEVD-FMK and Z-LEHD-FMK, but not nitric oxide synthase inhibitor Nomega-nitro-l-arginine methyl ester, significantly reduced the cell death-inducing effect of AEA. MK-886 72-77 arachidonate 5-lipoxygenase Homo sapiens 10-24 10864142-4 2000 Arachidonic acid-stimulated p38 MAPK phosphorylation was attenuated in cells pretreated with the Gi/o inhibitor (pertussis toxin), but not with the dual cyclooxygenase/lipoxygenase inhibitor (BW755C) or the leukotriene biosynthesis inhibitor (MK886). MK-886 243-248 mitogen activated protein kinase 14 Rattus norvegicus 28-31 10953307-0 2000 A genomic response of H-358 bronchiolar carcinoma cells to MK 886, an inhibitor of 5-lipoxygenase, assessed with a cDNA array. MK-886 59-65 arachidonate 5-lipoxygenase Homo sapiens 83-97 10600493-4 1999 Consistently, incubation of CHP100 cells with inhibitors of 5-lipoxygenase (5,8,11,14-eicosatetraynoic acid and MK886) reduced light emission and PCD, whereas inhibition of catalase by 3-amino-1, 2,4-triazole enhanced both processes. MK-886 112-117 arachidonate 5-lipoxygenase Homo sapiens 60-74 10588632-10 1999 Inhibition of 5-lipoxygenase (5-LO) with BWA4C and of 5-LO-activating protein (FLAP) with MK886 abolished GM-CSF- and DEX-induced neutrophil survival. MK-886 90-95 colony stimulating factor 2 Homo sapiens 106-112 10588632-11 1999 BWA4C and MK886 abolished GM-CSF- induced neotrophil survival in a concentration-dependent manner (1 nM to 10 microM), with IC(50) values of 182.0 nM and 63.1 nM, respectively. MK-886 10-15 colony stimulating factor 2 Homo sapiens 26-32 10493497-8 1999 The cyclooxygenase inhibitor aspirin and the 5-lipoxygenase inhibitor MK-886 both partially inhibited DNA synthesis in response to NNK. MK-886 70-76 arachidonate 5-lipoxygenase Homo sapiens 45-59 10422663-8 1999 Indomethacin abolished the incapacitation induced by CG in naive joints, but only the 5-lipoxygenase inhibitor MK-886 plus indomethacin blocked the response in primed joints. MK-886 111-117 arachidonate 5-lipoxygenase Rattus norvegicus 86-100 10628326-0 1999 Altered oncogene, tumor suppressor and cell-cycle gene expression in PANC-1 cells cultured with the pleiotrophic 5-lipoxygenase inhibitor, MK886, assessed with a gene chip. MK-886 139-144 arachidonate 5-lipoxygenase Homo sapiens 113-127 10422663-9 1999 MK-886 did not modify CG-induced incapacitation in naive joints, but lately reversed CG-induced incapacitation in primed joints, and blocked TNF alpha-induced response. MK-886 0-6 tumor necrosis factor Rattus norvegicus 141-150 10333477-0 1999 The 5-lipoxygenase-activating protein (FLAP) inhibitor, MK886, induces apoptosis independently of FLAP. MK-886 56-61 arachidonate 5-lipoxygenase activating protein Mus musculus 39-43 10333477-3 1999 Furthermore, the concentration of MK886, a FLAP inhibitor, required to induce apoptosis is approximately 100-fold more than that required to inhibit LOX, and this compound remains effective in cells lacking LOX. MK-886 34-39 arachidonate 5-lipoxygenase activating protein Mus musculus 43-47 10333477-4 1999 The present study examines the role of FLAP in MK886-induced apoptosis. MK-886 47-52 arachidonate 5-lipoxygenase activating protein Mus musculus 39-43 10333477-5 1999 MK886 induced apoptosis in WSU cells, a human chronic lymphocytic leukaemia cell line that lacks FLAP protein and mRNA, suggesting that this agent is acting independently of FLAP. MK-886 0-5 arachidonate 5-lipoxygenase activating protein Homo sapiens 97-101 10333477-9 1999 Furthermore, FLAP-depleted cells exhibited the same level of apoptosis 8 h after treatment with 10 microM MK886, as did control cells. MK-886 106-111 arachidonate 5-lipoxygenase activating protein Mus musculus 13-17 9845549-9 1998 Treatment of neutrophils with an inhibitor of 5-lipoxygenase-activating protein (MK886) and thus synthesis of leukotrienes (LTs) or with an antagonist of the LTB4 receptor (LY223982) blocked the release of elastase. MK-886 81-86 arachidonate 5-lipoxygenase Homo sapiens 46-60 10064732-7 1999 Additional support for a role of MRP1 in platelet LTC4 export was obtained by the findings that the process was inhibited by probenecid and the 5-lipoxygenase-activating protein (FLAP) inhibitor, MK-886. MK-886 196-202 ATP binding cassette subfamily C member 1 Homo sapiens 33-37 9887177-5 1999 MK-886 (1 mg/kg ip) administered 4 h before LPS efficaciously prevented LPS-induced hypothermia in mice. MK-886 0-6 toll-like receptor 4 Mus musculus 72-75 9774436-7 1998 bcl-xL and bcl-2 proteins, but not bax or FLAP, were decreased by 4 h after 5 nmol of MK886/10(6) cells in both cell lines, although the higher levels of bcl-xL in overexpressors took longer to disappear. MK-886 86-91 BCL2-like 1 Mus musculus 154-160 9792133-8 1998 MK886, a 5-lipoxygenase-inhibitor with a different mechanism of action, induced nonnecrotic changes largely confined to the cytoplasm, most consistent with type 2 "autophagic" programmed cell death. MK-886 0-5 arachidonate 5-lipoxygenase Homo sapiens 9-23 9774436-2 1998 The current study examined the expression of FLAP and bcl family proteins and the induction of apoptosis in interleukin-3-dependent control and bcl-xL-overexpressing FL5.12 cell lines after treatment with MK886, a specific FLAP inhibitor. MK-886 205-210 interleukin 3 Mus musculus 108-121 9774436-9 1998 Caspase-3 was activated 2 h after MK886 treatment in control cells but not in bcl-xL cells. MK-886 34-39 caspase 3 Mus musculus 0-9 9774436-2 1998 The current study examined the expression of FLAP and bcl family proteins and the induction of apoptosis in interleukin-3-dependent control and bcl-xL-overexpressing FL5.12 cell lines after treatment with MK886, a specific FLAP inhibitor. MK-886 205-210 BCL2-like 1 Mus musculus 144-150 9774436-10 1998 Inhibition of caspase-3 decreased MK886-induced apoptosis by 50% in control cells. MK-886 34-39 caspase 3 Mus musculus 14-23 9774436-2 1998 The current study examined the expression of FLAP and bcl family proteins and the induction of apoptosis in interleukin-3-dependent control and bcl-xL-overexpressing FL5.12 cell lines after treatment with MK886, a specific FLAP inhibitor. MK-886 205-210 arachidonate 5-lipoxygenase activating protein Mus musculus 223-227 9789062-6 1998 Inhibition of 5-lipoxygenase by MK886 completely blocks 5-HETE production and induces massive apoptosis in both hormone-responsive (LNCaP) and -nonresponsive (PC3) human prostate cancer cells. MK-886 32-37 arachidonate 5-lipoxygenase Homo sapiens 14-28 9774436-6 1998 A dose- and time-response study revealed that 5 nmol of MK886/10(6) cells was sufficient to induce apoptosis both in control and bcl-xL cells, respectively, but to different degrees. MK-886 56-61 BCL2-like 1 Mus musculus 129-135 9774436-7 1998 bcl-xL and bcl-2 proteins, but not bax or FLAP, were decreased by 4 h after 5 nmol of MK886/10(6) cells in both cell lines, although the higher levels of bcl-xL in overexpressors took longer to disappear. MK-886 86-91 BCL2-like 1 Mus musculus 0-6 9774436-7 1998 bcl-xL and bcl-2 proteins, but not bax or FLAP, were decreased by 4 h after 5 nmol of MK886/10(6) cells in both cell lines, although the higher levels of bcl-xL in overexpressors took longer to disappear. MK-886 86-91 B cell leukemia/lymphoma 2 Mus musculus 11-16 9774436-12 1998 These data indicate that MK886 induces extensive apoptosis that is partially caspase-3 dependent and may be related to a rapid loss of bcl-xL. MK-886 25-30 caspase 3 Mus musculus 77-86 9774436-12 1998 These data indicate that MK886 induces extensive apoptosis that is partially caspase-3 dependent and may be related to a rapid loss of bcl-xL. MK-886 25-30 BCL2-like 1 Mus musculus 135-141 9639560-4 1998 Consistent with this observation, selective inhibitors of prostaglandin H synthase (i.e. indomethacin) and 5-lipoxygenase (i.e. MK886 and caffeic acid) protected CHP100 cells against gp120-induced necrosis. MK-886 128-133 arachidonate 5-lipoxygenase Homo sapiens 107-121 9742967-4 1998 In addition, 5-lipoxygenase was activated by tamoxifen and the specific enzyme inhibitor, MK886, protected K562 cells against the drug. MK-886 90-95 arachidonate 5-lipoxygenase Homo sapiens 13-27 9639560-4 1998 Consistent with this observation, selective inhibitors of prostaglandin H synthase (i.e. indomethacin) and 5-lipoxygenase (i.e. MK886 and caffeic acid) protected CHP100 cells against gp120-induced necrosis. MK-886 128-133 inter-alpha-trypsin inhibitor heavy chain 4 Homo sapiens 183-188 9630716-4 1998 MK-886, a potent inhibitor of leukotriene biosynthesis, blocked the FLAP dependent S.t.LOX activation after preincubation with FLAP transfected membranes. MK-886 0-6 arachidonate 5-lipoxygenase activating protein Homo sapiens 68-72 9630716-4 1998 MK-886, a potent inhibitor of leukotriene biosynthesis, blocked the FLAP dependent S.t.LOX activation after preincubation with FLAP transfected membranes. MK-886 0-6 lysyl oxidase Homo sapiens 87-90 9630716-4 1998 MK-886, a potent inhibitor of leukotriene biosynthesis, blocked the FLAP dependent S.t.LOX activation after preincubation with FLAP transfected membranes. MK-886 0-6 arachidonate 5-lipoxygenase activating protein Homo sapiens 127-131 9585079-1 1998 MK-886, a specific inhibitor of 5-lipoxygenase inhibited DNA replication in leukemic HL-60 cells in a dose-dependent manner. MK-886 0-6 arachidonate 5-lipoxygenase Homo sapiens 32-46 9609743-5 1998 There was increased IL-8 nuclear factor-kappaB (NF-kappaB) DNA-binding activity after histamine stimulation, and this was inhibited by DPH and MK-886. MK-886 143-149 C-X-C motif chemokine ligand 8 Homo sapiens 20-24 9609743-5 1998 There was increased IL-8 nuclear factor-kappaB (NF-kappaB) DNA-binding activity after histamine stimulation, and this was inhibited by DPH and MK-886. MK-886 143-149 nuclear factor kappa B subunit 1 Homo sapiens 48-57 9555040-6 1998 Leukotriene synthesis in both eosinophils and neutrophils was suppressed by the 5-lipoxygenase activating protein (FLAP) inhibitor, MK-886. MK-886 132-138 arachidonate 5-lipoxygenase activating protein Equus caballus 115-119 9615721-1 1998 The 5-lipoxygenase inhibitors ETYA, SC41661A and MK886 reduced the proliferation and viability of Panc-1 human pancreatic cancer cells. MK-886 49-54 arachidonate 5-lipoxygenase Homo sapiens 4-18 9615721-11 1998 When gamma linolenic acid was combined with MK886, the more effective of the two 5-lipoxygenase inhibitors, a synergistic reduction in Panc-1 cell number and viability occurred. MK-886 44-49 arachidonate 5-lipoxygenase Homo sapiens 81-95 9696418-3 1998 It was clearly demonstrated that two structurally different inhibitors of 5-lipoxygenase metabolism, i.e., 3-[1-(4-chlorobenzyl)-3-t-butyl-thio-5-isopropylindol-2-yl]-2,2-di methyl propanoic acid (MK-886) and esculetin, significantly potentiated the HL-60 cell differentiation induced by retinoic acid or DMSO. MK-886 107-195 arachidonate 5-lipoxygenase Homo sapiens 74-88 9696418-3 1998 It was clearly demonstrated that two structurally different inhibitors of 5-lipoxygenase metabolism, i.e., 3-[1-(4-chlorobenzyl)-3-t-butyl-thio-5-isopropylindol-2-yl]-2,2-di methyl propanoic acid (MK-886) and esculetin, significantly potentiated the HL-60 cell differentiation induced by retinoic acid or DMSO. MK-886 197-203 arachidonate 5-lipoxygenase Homo sapiens 74-88 9550202-9 1998 5-lipoxygenase inhibitor MK-886 (100 nM) lifts the inhibitory effect of arachidonate. MK-886 25-31 arachidonate 5-lipoxygenase Homo sapiens 0-14 9497404-5 1998 Using MK886, a specific inhibitor of the enzymatic pathway that leads to the augmentation of IM by SST, we have uncovered and characterized a second conductance activated by the peptide. MK-886 6-11 somatostatin Rattus norvegicus 99-102 9497404-7 1998 In the presence of MK886, SST elicited an outward current that reversed around -100 mV and that displayed a linear current-voltage relationship. MK-886 19-24 somatostatin Rattus norvegicus 26-29 9531055-0 1998 Suppression of intimal hyperplasia by a 5-lipoxygenase inhibitor, MK-886: studies with a photochemical model of endothelial injury. MK-886 66-72 arachidonate 5-lipoxygenase Rattus norvegicus 40-54 9531055-6 1998 In cultured rat-derived smooth muscle cells, LTB4, an active metabolite of 5-lipoxygenase whose biosynthesis in air pouch exudate was suppressed by MK-886, stimulated cell migration. MK-886 148-154 arachidonate 5-lipoxygenase Rattus norvegicus 75-89 9066788-9 1997 When IL-3 is added in the presence of any of three lipoxygenase inhibitors tested (Piriprost, caffeic acid, nordihydroguiaretic acid) or FLAP inhibitor, MK-886, there is dose-dependent inhibition of the resumption of proliferation and of DNA synthesis. MK-886 153-159 interleukin 3 Homo sapiens 5-9 9359857-4 1997 Metabolism to 14, 15-dehydro-LTC4 is inhibited by MK-886, a reported LTC4 synthase inhibitor in human platelets, with a potency comparable with that shown by LTA4. MK-886 50-56 leukotriene C4 synthase Homo sapiens 69-82 9372685-5 1997 The PAF-elicited bronchoconstriction in the transgenic mice was significantly reduced not only by a PAF receptor antagonist (WEB-2086) but also by a thromboxane synthesis inhibitor (indomethacin or ozagrel), an inhibitor of 5-lipoxygenase-activating protein (MK-886), or a cysteinyl leukotriene (LT) antagonist (pranlukast). MK-886 259-265 patchy fur Mus musculus 4-7 9440240-9 1997 Previous injections of inhibitors of 5-lipoxygenase (MK-886) or cyclooxygenase (aspirin or indomethacin) significantly decreased the magnitude of the lung oedema induced by scorpion venom. MK-886 53-59 arachidonate 5-lipoxygenase Rattus norvegicus 37-51 9349629-4 1997 Different leukotriene biosynthesis inhibitors like the nonredox type inhibitor ZM 230487, the redox type inhibitor BW A4C and the FLAP inhibitor MK886 were tested and the results were compared with an assay system based on normal human granulocytes. MK-886 145-150 arachidonate 5-lipoxygenase activating protein Homo sapiens 130-134 9209681-7 1997 LTC4 synthase activity was inhibited by the addition of MK-886, and was not altered by treatment with N-ethylmaleimide or 1-chloro-2,4-dinitrobenzene. MK-886 56-62 leukotriene C4 synthase Homo sapiens 0-13 9101418-8 1997 Pretreatment with either the cycloxygenase inhibitor indomethacin or the 5-lipoxygenase inhibitor L-663,536 had no effect on TNF levels. MK-886 98-107 arachidonate 5-lipoxygenase Rattus norvegicus 73-87 9113110-4 1997 We report that human platelet LTC4-S was inhibited by MK-886 and BAY-X1005 (IC50 of 4.7 microM and 91.2 microM, respectively), but not by zileuton (inactive up to 300 microM); all 3 compounds were able to inhibit 5-lipoxygenase metabolite biosynthesis in intact human polymorphonuclear leukocytes (IC50 of 0.044 microM, 0.85 microM, and 1.5 microM, respectively). MK-886 54-60 leukotriene C4 synthase Homo sapiens 30-36 9119028-14 1997 Finally, the prior treatment of astrocytes with MK886, a 5-lipoxygenase-activating protein inhibitor, prevented JNK from stimulation, but did not prevent thymidine incorporation from inhibition, both induced by H2O2. MK-886 48-53 mitogen-activated protein kinase 8 Homo sapiens 112-115 9435558-5 1997 However, significant inhibition was noted after treatment with either MK-886 (5-lipoxygenase inhibitor) or a nitric oxide (NO) donor (diethylenetriamine/NO). MK-886 70-76 arachidonate 5-lipoxygenase Homo sapiens 78-92 9353042-6 1997 Treatment of PNG with the leukotriene-B4 inhibitor MK-886 prior to stimulation with M. tuberculosis or LAM partially blocked IL-8 and GRO-alpha induction, suggesting involvement of the 5-lipoxygenase pathway in the secretion of these chemokines. MK-886 51-57 C-X-C motif chemokine ligand 8 Homo sapiens 125-129 9431445-9 1997 Structurally diverse FLAP inhibitors tested against LTC4 synthase were all micromolar inhibitors of the enzyme over a 10-fold range, with MK-886 at 11 microM. MK-886 138-144 leukotriene C4 synthase Homo sapiens 52-65 9261338-1 1997 It was clearly demonstrated that two structurally different inhibitors of 5-lipoxygenase (5-LPO) metabolism (leukotriene synthesis), i.e. MK-886 and esculetin, when combined with transforming growth factor-beta 1 (TGF-beta 1), significantly enhanced the differentiation but did not change proliferation (i.e. cell number and cell cycle parameters) of human leukemia HL-60 cells in vitro. MK-886 138-144 arachidonate 5-lipoxygenase Homo sapiens 74-88 9261338-1 1997 It was clearly demonstrated that two structurally different inhibitors of 5-lipoxygenase (5-LPO) metabolism (leukotriene synthesis), i.e. MK-886 and esculetin, when combined with transforming growth factor-beta 1 (TGF-beta 1), significantly enhanced the differentiation but did not change proliferation (i.e. cell number and cell cycle parameters) of human leukemia HL-60 cells in vitro. MK-886 138-144 lactoperoxidase Homo sapiens 92-95 9261338-1 1997 It was clearly demonstrated that two structurally different inhibitors of 5-lipoxygenase (5-LPO) metabolism (leukotriene synthesis), i.e. MK-886 and esculetin, when combined with transforming growth factor-beta 1 (TGF-beta 1), significantly enhanced the differentiation but did not change proliferation (i.e. cell number and cell cycle parameters) of human leukemia HL-60 cells in vitro. MK-886 138-144 transforming growth factor beta 1 Homo sapiens 179-212 9261338-2 1997 Although cell morphology and measurement of cell surface antigens (CD11b, CD14, and CD66b) after 48 h of combined treatment with MK-886 and TGF-beta 1 suggested a shift of the HL-60 cell population into more differentiated stages of myelopoiesis, cells with a fully mature phenotype were not observed. MK-886 129-135 CEA cell adhesion molecule 8 Homo sapiens 84-89 9261338-5 1997 The differentiation effects of TGF-beta 1 alone and especially of its combination with MK-886 were most pronounced when the cells were pretreated with dimethyl sulfoxide or all-trans-retinoic acid. MK-886 87-93 transforming growth factor beta 1 Homo sapiens 31-41 9103531-4 1997 The data show that the dual inhibition of 5-lipoxygenase and HLE is unique to boswellic acids: other pentacyclic triterpenes with HLE inhibitory activities (e.g., ursolic acid and amyrin) do not inhibit 5-lipoxygenase, and leukotriene biosynthesis inhibitors from different chemical classes (e.g., NDGA, MK-886 and ZM-230,487) do not impair HLE activity. MK-886 304-310 arachidonate 5-lipoxygenase Homo sapiens 42-56 9103531-4 1997 The data show that the dual inhibition of 5-lipoxygenase and HLE is unique to boswellic acids: other pentacyclic triterpenes with HLE inhibitory activities (e.g., ursolic acid and amyrin) do not inhibit 5-lipoxygenase, and leukotriene biosynthesis inhibitors from different chemical classes (e.g., NDGA, MK-886 and ZM-230,487) do not impair HLE activity. MK-886 304-310 elastase, neutrophil expressed Homo sapiens 61-64 8912128-7 1996 Repeated prior dosing up to 5 h with the novel five lipoxygenase activating protein (FLAP) inhibitor, MK886 (50 and 100 mg/kg), reduced the lesions developed by indomethacin (30 mg/kg, s.c.). MK-886 102-107 arachidonate 5-lipoxygenase activating protein Rattus norvegicus 85-89 9044439-1 1997 Micromolar MK886, a selective inhibitor of 5-lipoxygenase at nanomolar concentration, induces physiologic cell death in U937 and chronic myelogenous leukemia blast cells. MK-886 11-16 arachidonate 5-lipoxygenase Homo sapiens 43-57 8917119-7 1996 Dexamethasone and MK 886 blocked the eosinophil migration induced by both the supernatants of saline-stimulated mast cells or macrophages and by IL-5 or IL-8. MK-886 18-24 interleukin 5 Rattus norvegicus 145-149 8647941-6 1996 A FLAP ligand, 3-[l-(4-chlorobenzyl)-3-t-butyl-thio-t-isopropylindol-2-yl]-2,2- dimethylpropanoic acid (MK-886), inhibited the acute angiotensin II and hypoxia-induced pulmonary vasoconstriction in vitro and the development of chronic hypoxic pulmonary hypertension in rats in vivo. MK-886 104-110 arachidonate 5-lipoxygenase activating protein Rattus norvegicus 2-6 8917356-0 1996 An in vivo inhibitor of 5-lipoxygenase, MK886, at micromolar concentration induces apoptosis in U937 and CML cells. MK-886 40-45 arachidonate 5-lipoxygenase Homo sapiens 24-38 8917356-1 1996 MK886 (Merck Frosst) is a selective in vivo inhibitor of 5-lipoxygenase, active at nanomolar concentrations. MK-886 0-5 arachidonate 5-lipoxygenase Homo sapiens 57-71 8917356-8 1996 Since MK886 inhibits the association of arachidonic acid with the 5-lipoxygenase activating protein, altered arachidonic acid metabolism may have contributed to these results. MK-886 6-11 arachidonate 5-lipoxygenase Homo sapiens 66-80 8814263-8 1996 Surprisingly, the inhibitor of leukotriene synthesis MK-886 in the range of concentration 1-10 microM inhibited CINC-1 induction by a mechanism that appears to be independent of its effect on eicosanoid production. MK-886 53-59 C-X-C motif chemokine ligand 1 Rattus norvegicus 112-118 8706658-9 1996 The 5-lipoxygenase-activating-protein inhibitor, MK-886, was active against both human and mouse recombinant leukotriene C4 synthase with IC50 values of 3.1 microM and 2.7 microM respectively. MK-886 49-55 leukotriene C4 synthase Mus musculus 109-132 8581269-19 1995 Like the coronary vascular effects of PAF, the effects of H-PAF and E-PAF were blocked by a PAF antagonist (FR-900452) and a leukotriene synthesis inhibitor (MK-886). MK-886 158-164 PCNA clamp associated factor Rattus norvegicus 60-63 8666909-5 1996 Lipid body induction by PAF required 5-lipoxygenase (LO) activity and was inhibited by the 5-lipoxygenase-activating protein antagonist MK 886 and the 5-LO inhibitor zileuton, but not by cyclooxygenase inhibitors. MK-886 136-142 patchy fur Mus musculus 24-27 8666909-5 1996 Lipid body induction by PAF required 5-lipoxygenase (LO) activity and was inhibited by the 5-lipoxygenase-activating protein antagonist MK 886 and the 5-LO inhibitor zileuton, but not by cyclooxygenase inhibitors. MK-886 136-142 arachidonate 5-lipoxygenase Mus musculus 91-105 8634114-9 1996 LPS-stimulated TNF-alpha releases from control and smoke-exposed AM were suppressed by phosphodiesterase inhibitors pentoxifylline and theophylline, and were enhanced by the lipoxygenase inhibitor, MK886. MK-886 198-203 tumor necrosis factor Oryctolagus cuniculus 15-24 8634114-9 1996 LPS-stimulated TNF-alpha releases from control and smoke-exposed AM were suppressed by phosphodiesterase inhibitors pentoxifylline and theophylline, and were enhanced by the lipoxygenase inhibitor, MK886. MK-886 198-203 polyunsaturated fatty acid lipoxygenase ALOX15 Oryctolagus cuniculus 174-186 8522947-6 1996 Moreover, electrophysiological experiments show that selective inhibition of FLAP with the compound MK-886 (0.25-1 microM) prevents the somatostatin-induced augmentation of the hippocampal K+ M-current. MK-886 100-106 arachidonate 5-lipoxygenase activating protein Rattus norvegicus 77-81 8722494-11 1996 MK-886 also inhibited synovial production of two other pleiotrophic cytokines which it regulates, IL-6 and IL-8. MK-886 0-6 interleukin 6 Homo sapiens 98-102 8722494-11 1996 MK-886 also inhibited synovial production of two other pleiotrophic cytokines which it regulates, IL-6 and IL-8. MK-886 0-6 C-X-C motif chemokine ligand 8 Homo sapiens 107-111 8581269-12 1995 Pretreatment with FR-900452 (a PAF receptor antagonist) or MK-886 (a leukotriene synthesis inhibitor) significantly reduced the vasodilator and vasoconstrictor effects of H-PAF and E-PAF. MK-886 59-65 PCNA clamp associated factor Rattus norvegicus 173-176 8581269-12 1995 Pretreatment with FR-900452 (a PAF receptor antagonist) or MK-886 (a leukotriene synthesis inhibitor) significantly reduced the vasodilator and vasoconstrictor effects of H-PAF and E-PAF. MK-886 59-65 PCNA clamp associated factor Rattus norvegicus 173-176 8581269-19 1995 Like the coronary vascular effects of PAF, the effects of H-PAF and E-PAF were blocked by a PAF antagonist (FR-900452) and a leukotriene synthesis inhibitor (MK-886). MK-886 158-164 PCNA clamp associated factor Rattus norvegicus 60-63 8581269-19 1995 Like the coronary vascular effects of PAF, the effects of H-PAF and E-PAF were blocked by a PAF antagonist (FR-900452) and a leukotriene synthesis inhibitor (MK-886). MK-886 158-164 PCNA clamp associated factor Rattus norvegicus 60-63 7556168-6 1995 Furthermore, MK886, the FLAP-binding cellular leukotriene biosynthesis inhibitor, reduced both LTB4 and 5-HETE formation. MK-886 13-18 arachidonate 5-lipoxygenase activating protein Homo sapiens 24-28 8551795-7 1995 Characteristic ultrastructural changes of apoptosis were seen at 120 h. MK886, an inhibitor of 5-lipoxygenase with a mechanism of action distinct from oxidation/reduction reagents, at 20-40 microM also inhibited CML and U937 cell proliferation and induced apoptosis, as shown by DNA laddering and ultrastructure. MK-886 72-77 arachidonate 5-lipoxygenase Homo sapiens 95-109 8774948-6 1995 Two selective inhibitors of 5-lipoxygenase, i.e. MK886 (5 mumol/l) and BAY X1005 (1 mumol/l), also enhanced the effect of TPA (10 nmol/l) without affecting the basal expression of the gene. MK-886 49-54 arachidonate 5-lipoxygenase Rattus norvegicus 28-42 7603462-3 1995 The presence of the noninhibitory pentacyclic triterpenes both in intact cells and in the cell-free system caused a concentration-dependent reversal of the 5-lipoxygenase inhibition by acetyl-11-keto-beta-boswellic acid, whereas the inhibitory actions of 5-lipoxygenase inhibitors from different chemical classes (MK-886, L-739,010, ZM-230,487, and nordihydroguaiaretic acid) were not modified. MK-886 314-320 arachidonate 5-lipoxygenase Rattus norvegicus 156-170 7669639-1 1995 MK-886, a leukotriene biosynthesis inhibitor, which prevents the translocation and activation of 5-lipoxygenase, has been proposed as an effective drug for the treatment of inflammatory disorders, including psoriasis. MK-886 0-6 arachidonate 5-lipoxygenase Homo sapiens 97-111 7669639-4 1995 Further investigations on the mechanism of action revealed that, in contrast with trifluoperazine, calmodulin antagonism by MK-886 in vitro is likely to be mediated at the level of the allosteric calmodulin-recognition site of phosphodiesterase, rather than by binding to calmodulin itself. MK-886 124-130 calmodulin 1 Homo sapiens 99-109 7669639-4 1995 Further investigations on the mechanism of action revealed that, in contrast with trifluoperazine, calmodulin antagonism by MK-886 in vitro is likely to be mediated at the level of the allosteric calmodulin-recognition site of phosphodiesterase, rather than by binding to calmodulin itself. MK-886 124-130 calmodulin 1 Homo sapiens 196-206 7669639-4 1995 Further investigations on the mechanism of action revealed that, in contrast with trifluoperazine, calmodulin antagonism by MK-886 in vitro is likely to be mediated at the level of the allosteric calmodulin-recognition site of phosphodiesterase, rather than by binding to calmodulin itself. MK-886 124-130 calmodulin 1 Homo sapiens 196-206 7840141-3 1995 In contrast, Thap had very little effect on the activation of PLA2 when 5-lipoxygenase (5-LO) was blocked by BW755C or MK-886, whereas A-23187 caused a substantial activation. MK-886 119-125 arachidonate 5-lipoxygenase Homo sapiens 72-86 7738170-8 1995 The effects of MK-886, which binds to FLAP, were examined in ionophore-stimulated AM and PBL. MK-886 15-21 arachidonate 5-lipoxygenase activating protein Homo sapiens 38-42 7484419-12 1995 MK-886, which inhibits the translocation of 5-lipoxygenase (5-LO) from the cytosol and its binding to the membranal 5-LO activating enzyme, suppressed dose-dependently follicular rupture from the treated ovary. MK-886 0-6 arachidonate 5-lipoxygenase Homo sapiens 44-58 8052639-10 1994 Moreover, LTC4 synthase is inhibitable by a FLAP inhibitor, MK-886. MK-886 60-66 arachidonate 5-lipoxygenase activating protein Homo sapiens 44-48 7741044-3 1994 The 5-LOX selective and orally active quinoline LSI, BAY X 1005, shares many mechanistic features with the indole LSI, MK-886. MK-886 119-125 lysyl oxidase Homo sapiens 6-9 8058773-2 1994 Treatment with either Zileuton (a specific reversible competitive inhibitor of 5-lipoxygenase) or MK886 (a specific irreversible inhibitor of the 5-lipoxygenase activator protein) prevented stimulated neutrophil adherence and chemotaxis (but not superoxide anion production) in vitro. MK-886 98-103 arachidonate 5-lipoxygenase Homo sapiens 146-160 18475674-5 1995 In the heart, the leukotriene synthesis inhibitor MK-886 (0.3 muM) significantly reduced the maximal effects to angiotensin II, but the leukotriene antagonist FPL 55712 (0.1 and 0.3 muM) had no effect. MK-886 50-56 angiotensinogen Rattus norvegicus 112-126 8052639-10 1994 Moreover, LTC4 synthase is inhibitable by a FLAP inhibitor, MK-886. MK-886 60-66 leukotriene C4 synthase Homo sapiens 10-23 8114000-10 1994 However, BAY x1005 or MK-886 in the presence of indomethacin prevented the increase in LTE4 levels that were observed during anti-IgE challenge. MK-886 22-28 immunoglobulin heavy constant epsilon Homo sapiens 130-133 8049076-5 1994 The FLAP inhibitor MK-886 was unable to block leukotriene synthesis from exogenous AA in the two cell types, despite its ability to completely inhibit 5-LO metabolism of endogenous AA. MK-886 19-25 arachidonate 5-lipoxygenase activating protein Homo sapiens 4-8 8031320-4 1994 At first sight this finding was not surprising since we have shown earlier that in intact cells this class of quinoline derivatives shares the same mode of action as MK-886, i.e. an indirect inhibition of 5-LOX activity by binding to FLAP. MK-886 166-172 lysyl oxidase Homo sapiens 207-210 8283057-3 1994 The enhanced renal production of leukotrienes observed in allograft recipients was reduced in a dose-dependent manner by the specific 5-lipoxygenase inhibitor MK886. MK-886 159-164 arachidonate 5-lipoxygenase Rattus norvegicus 134-148 8279553-6 1993 This response was blocked by the dual inhibitor of cyclooxygenase and lipoxygenases, BW755C (2 x 10(-5)-2 x 10(-4) M), by the selective 5-lipoxygenase inhibitor L-651,392 (10(-7)-10(-5) M), and by MK-886 (10(-9)-10(-7) M), which blocks translocation of 5-lipoxygenase. MK-886 197-203 arachidonate 5-lipoxygenase Rattus norvegicus 136-150 8245474-8 1993 Finally, pertussis toxin and the 5-LO translocation inhibitor, MK-886, both blocked the IL-8-elicited 5-LO activation. MK-886 63-69 C-X-C motif chemokine ligand 8 Homo sapiens 88-92 8268454-3 1993 Zileuton and MK-886 (10 microM) significantly inhibited the dose-related contraction to anti-IgE as compared with solvent (DMSO). MK-886 13-19 immunoglobulin heavy constant epsilon Homo sapiens 93-96 8245690-4 1993 The same effect was observed after treatment of rats with the arachidonate 5-lipoxygenase inhibitor MK886. MK-886 100-105 arachidonate 5-lipoxygenase Rattus norvegicus 62-89 8357992-4 1993 Pretreatment with the arachidonate 5-lipoxygenase inhibitor MK-886 partially ameliorated the decrements in GFR and RBF, reduced the glomerular leukocyte infiltration and completely inhibited the glomerular LTB4 synthesis. MK-886 60-66 arachidonate 5-lipoxygenase Rattus norvegicus 22-49 8344271-5 1993 LT synthesis in cells coexpressing FLAP and 5-LO is inhibited by 3-[1-(p-chlorophenyl)-5-isopropyl-3-tert-butylthio-1H-indol-2-yl]-2,2- dimethyl-propanoic acid (MK-886), an LT biosynthesis inhibitor which specifically binds to FLAP. MK-886 161-167 arachidonate 5-lipoxygenase activating protein Homo sapiens 35-39 8498596-6 1993 Treatment with the 5"-lipoxygenase inhibitor MK-886 significantly reduced concentrations of leukotriene B4 in the colon of TNBE-treated rats but did not affect food intake. MK-886 45-51 arachidonate 5-lipoxygenase Rattus norvegicus 19-34 8385430-5 1993 MK-886 significantly inhibited the EAR by 58.4% (AUC0-3 h) and the LAR by 43.6% (AUC3-7 h) when compared with placebo (p < 0.01). MK-886 0-6 protein tyrosine phosphatase receptor type F Homo sapiens 67-70 8384212-7 1993 Two structurally different LTD4 receptor antagonists, MK-571 and ICI 204,219, also competed for 125I-azido-LTD4 specific binding with nanomolar potency, whereas the leukotriene synthesis inhibitor, MK-886, was 10,000-fold less active. MK-886 198-204 cysteinyl leukotriene receptor 1 Cavia porcellus 27-40 8358023-8 1993 The synthesis of these products was inhibited by MK-886, a compound which specifically binds to FLAP. MK-886 49-55 arachidonate 5-lipoxygenase activating protein Homo sapiens 96-100 8440384-4 1993 This binding is inhibited by both arachidonic acid and MK-886, an LT biosynthesis inhibitor which specifically interacts with FLAP. MK-886 55-61 arachidonate 5-lipoxygenase activating protein Homo sapiens 126-130 1331218-6 1992 Inhibition of 5-lipoxygenase pathway by AA-861 or MK 886 inhibited the PAF-induced augmentation of both IL-6 and LTB4 production, suggesting an implication of endogenous leukotrienes in this mechanism. MK-886 50-56 arachidonate 5-lipoxygenase Rattus norvegicus 14-28 8273563-2 1993 MK886, L-656,224, PF-5901, and tepoxalin all inhibited IL-1 production in concentrations up to 10 microM, whereas other 5-LO inhibitors (ICI-211,965, zileuton), as well as IL-1 synthesis inhibitors (IX-207,887, tenidap), were inactive. MK-886 0-5 interleukin 1 alpha Homo sapiens 55-59 8273581-3 1993 The oral administration of A-64077 and MK-886, two 5-lipoxygenase inhibitors (5-LOIs), at 10 mg/kg causes marked decreases in LTB4 release at the above-mentioned time intervals. MK-886 39-45 arachidonate 5-lipoxygenase Rattus norvegicus 51-65 8419261-6 1993 These alterations were significantly (P < 0.05) reduced by daily treatment with MK-886, a 5-lipoxygenase inhibitor (10 mg/kg, orally), whereas indomethacin (1 mg/kg per day, intramuscularly) was ineffective. MK-886 83-89 arachidonate 5-lipoxygenase Rattus norvegicus 93-107 1335586-4 1992 Thus, the order of potency was MK-886 > BI-L-239 > A-64077 for inhibition of calcium ionophore-induced LTB4 generation. MK-886 31-37 prostaglandin reductase 1 Cavia porcellus 109-113 1429555-4 1992 Accumulation of active membrane-associated 5-lipoxygenase was inhibited and reversed by the 5-lipoxygenase translocation inhibitor MK-886. MK-886 131-137 arachidonate 5-lipoxygenase Homo sapiens 43-57 1429555-4 1992 Accumulation of active membrane-associated 5-lipoxygenase was inhibited and reversed by the 5-lipoxygenase translocation inhibitor MK-886. MK-886 131-137 arachidonate 5-lipoxygenase Homo sapiens 92-106 1429555-7 1992 The ability to metabolize hydroxy fatty acids was dependent upon 5-lipoxygenase-activating protein association, but was lost if 5-lipoxygenase was eluted from the membrane by MK-886. MK-886 175-181 arachidonate 5-lipoxygenase Homo sapiens 128-142 1331218-6 1992 Inhibition of 5-lipoxygenase pathway by AA-861 or MK 886 inhibited the PAF-induced augmentation of both IL-6 and LTB4 production, suggesting an implication of endogenous leukotrienes in this mechanism. MK-886 50-56 PCNA clamp associated factor Rattus norvegicus 71-74 1331218-6 1992 Inhibition of 5-lipoxygenase pathway by AA-861 or MK 886 inhibited the PAF-induced augmentation of both IL-6 and LTB4 production, suggesting an implication of endogenous leukotrienes in this mechanism. MK-886 50-56 interleukin 6 Rattus norvegicus 104-108 1400062-9 1992 The 5-lipoxygenase-activating protein inhibitor MK886, administered orally 2-6 h before perfusion, also inhibited the pressor response to PAF as well as LT production, as did DEC. We conclude that 1) the extended pulmonary hypertension induced by PAF was caused mainly by prolonged activation of 5-lipoxygenase with LTC4 production, 2) the relative overall lung clearance of LTB4, LTD4, and LTE4 was slower than that of LTC4, and 3) LTB4, LTD4, and LTE4 had no appreciable pressor effect. MK-886 48-53 arachidonate 5-lipoxygenase Rattus norvegicus 4-18 1400062-9 1992 The 5-lipoxygenase-activating protein inhibitor MK886, administered orally 2-6 h before perfusion, also inhibited the pressor response to PAF as well as LT production, as did DEC. We conclude that 1) the extended pulmonary hypertension induced by PAF was caused mainly by prolonged activation of 5-lipoxygenase with LTC4 production, 2) the relative overall lung clearance of LTB4, LTD4, and LTE4 was slower than that of LTC4, and 3) LTB4, LTD4, and LTE4 had no appreciable pressor effect. MK-886 48-53 PCNA clamp associated factor Rattus norvegicus 138-141 1400062-9 1992 The 5-lipoxygenase-activating protein inhibitor MK886, administered orally 2-6 h before perfusion, also inhibited the pressor response to PAF as well as LT production, as did DEC. We conclude that 1) the extended pulmonary hypertension induced by PAF was caused mainly by prolonged activation of 5-lipoxygenase with LTC4 production, 2) the relative overall lung clearance of LTB4, LTD4, and LTE4 was slower than that of LTC4, and 3) LTB4, LTD4, and LTE4 had no appreciable pressor effect. MK-886 48-53 PCNA clamp associated factor Rattus norvegicus 247-250 1400062-9 1992 The 5-lipoxygenase-activating protein inhibitor MK886, administered orally 2-6 h before perfusion, also inhibited the pressor response to PAF as well as LT production, as did DEC. We conclude that 1) the extended pulmonary hypertension induced by PAF was caused mainly by prolonged activation of 5-lipoxygenase with LTC4 production, 2) the relative overall lung clearance of LTB4, LTD4, and LTE4 was slower than that of LTC4, and 3) LTB4, LTD4, and LTE4 had no appreciable pressor effect. MK-886 48-53 arachidonate 5-lipoxygenase Rattus norvegicus 296-310 1314503-4 1992 In contrast, LTB4 release correlated with the translocation of 5-lipoxygenase from the cytosol to the membrane fraction of the cells following A23187 stimulation and was inhibited by MK-886. MK-886 183-189 arachidonate 5-lipoxygenase Homo sapiens 63-77 1610790-6 1992 Using specific lipoxygenase inhibitors L-656,224 and MK 886, we found inhibition of GnRH-induced LH release by about 40% at concentrations known to specifically inhibit the 5-lipoxygenase pathway. MK-886 53-59 gonadotropin releasing hormone 1 Rattus norvegicus 84-88 1610790-6 1992 Using specific lipoxygenase inhibitors L-656,224 and MK 886, we found inhibition of GnRH-induced LH release by about 40% at concentrations known to specifically inhibit the 5-lipoxygenase pathway. MK-886 53-59 arachidonate 5-lipoxygenase Rattus norvegicus 173-187 1857337-1 1991 An indole class of leukotriene synthesis inhibitors, exemplified by MK-886, which does not directly inhibit 5-lipoxygenase, has been shown to bind to an 18-kDa leukocyte membrane protein and to inhibit 5-lipoxygenase membrane translocation. MK-886 68-74 arachidonate 5-lipoxygenase Homo sapiens 202-216 1748650-3 1991 In addition, we have shown inhibition of A23187- and fMLP-induced 5-lipoxygenase translocation by an indole and a quinoline leukotriene synthesis inhibitor, MK-886 and L-674,573, respectively. MK-886 157-163 formyl peptide receptor 1 Homo sapiens 53-57 1748650-3 1991 In addition, we have shown inhibition of A23187- and fMLP-induced 5-lipoxygenase translocation by an indole and a quinoline leukotriene synthesis inhibitor, MK-886 and L-674,573, respectively. MK-886 157-163 arachidonate 5-lipoxygenase Homo sapiens 66-80 1783470-4 1991 When the protective potency of the specific 5-lipoxygenase inhibitors (MK 886, CGS 81585) was tested in endotoxin-induced leukopenia and shock, they were found to be ineffective. MK-886 71-77 arachidonate 5-lipoxygenase Mus musculus 44-58 1652337-9 1991 However L-649,923 (a leukotriene antagonist) and MK-886 (a leukotriene synthesis inhibitor) eliminated both the vasodilator and vasoconstrictor effects of PAF. MK-886 49-55 PCNA clamp associated factor Rattus norvegicus 155-158 1900463-6 1991 These data also indicate that MK-886, a novel inhibitor of 5-lipoxygenase product formation, is a potentially useful leukotriene inhibitor which does not affect monokine production. MK-886 30-36 arachidonate 5-lipoxygenase Homo sapiens 59-73 1846160-9 1991 LTB4 release in response to all stimuli tested was inhibited by MK-886, a drug that binds to 5-lipoxygenase-activating protein. MK-886 64-70 arachidonate 5-lipoxygenase Homo sapiens 93-107 1793062-6 1991 The mechanism of action of MK-886 has been found to be the inhibition of activation of the 5-lipoxygenase enzyme. MK-886 27-33 arachidonate 5-lipoxygenase Homo sapiens 91-105 1650523-6 1991 The selective 5-lipoxygenase inhibitors, ICI207968, A64077 and BWA4C, and the 5-lipoxygenase translocation inhibitor MK886, decreased leukotriene generation but enhanced TNF production. MK-886 117-122 arachidonate 5-lipoxygenase Rattus norvegicus 78-92 1650523-6 1991 The selective 5-lipoxygenase inhibitors, ICI207968, A64077 and BWA4C, and the 5-lipoxygenase translocation inhibitor MK886, decreased leukotriene generation but enhanced TNF production. MK-886 117-122 tumor necrosis factor Rattus norvegicus 170-173 1899837-6 1991 LTC4 transport was inhibited by LTD4 receptor antagonists (IC50 = 1.0 microM for MK-571 and 1.3 microM for LY245769) and by the inhibitor of leukotriene biosynthesis MK-886 (IC50 = 1.8 microM). MK-886 166-172 cysteinyl leukotriene receptor 1 Homo sapiens 32-45 2174053-4 1990 Cellular leukotriene synthesis in this system is functionally dependent on FLAP as shown by its inhibition by the leukotriene biosynthesis inhibitor MK-886, a compound which specifically binds to FLAP. MK-886 149-155 arachidonate 5-lipoxygenase activating protein Homo sapiens 75-79 2174053-4 1990 Cellular leukotriene synthesis in this system is functionally dependent on FLAP as shown by its inhibition by the leukotriene biosynthesis inhibitor MK-886, a compound which specifically binds to FLAP. MK-886 149-155 arachidonate 5-lipoxygenase activating protein Homo sapiens 196-200 22654897-2 2012 We found free fatty acid accumulation, enhanced three acyl-CoA dehydrogenases, catalyzing the first reaction in the beta-oxidation system and being assumed to have normal activities in these patients, and PPARalpha activation that was confirmed in the experiments using MK886, a PPARalpha specific antagonist and fenofibrate, a PPARalpha specific agonist. MK-886 270-275 peroxisome proliferator activated receptor alpha Homo sapiens 205-214 2164857-2 1990 We have investigated the inhibitory activity of compound MK-886 (formerly L-663,536), an indole derivative, on 5-lipoxygenase product synthesis in various human phagocytes stimulated with either the ionophore A23187, in the presence and absence of exogenous arachidonic acid, or platelet-activating factor (PAF). MK-886 57-63 arachidonate 5-lipoxygenase Homo sapiens 111-125 30219501-6 2018 However, we ruled out this possibility as OEA- (but not OLDA-) excitation was abolished by the PPAR (peroxisome proliferator activated receptor) alpha antagonist MK886. MK-886 162-167 peroxisome proliferator activated receptor alpha Mus musculus 95-99 30219501-6 2018 However, we ruled out this possibility as OEA- (but not OLDA-) excitation was abolished by the PPAR (peroxisome proliferator activated receptor) alpha antagonist MK886. MK-886 162-167 peroxisome proliferator activated receptor alpha Mus musculus 101-150 2164857-8 1990 MK-886 inhibited 5-lipoxygenase product synthesis in A23187-stimulated blood eosinophils and monocytes, and in neutrophils primed with granulocyte-macrophage colony-stimulating factor and stimulated with PAF with IC50 values of 1-13 nM. MK-886 0-6 arachidonate 5-lipoxygenase Homo sapiens 17-31 2164857-8 1990 MK-886 inhibited 5-lipoxygenase product synthesis in A23187-stimulated blood eosinophils and monocytes, and in neutrophils primed with granulocyte-macrophage colony-stimulating factor and stimulated with PAF with IC50 values of 1-13 nM. MK-886 0-6 colony stimulating factor 2 Homo sapiens 135-183 2164857-8 1990 MK-886 inhibited 5-lipoxygenase product synthesis in A23187-stimulated blood eosinophils and monocytes, and in neutrophils primed with granulocyte-macrophage colony-stimulating factor and stimulated with PAF with IC50 values of 1-13 nM. MK-886 0-6 PCNA clamp associated factor Homo sapiens 204-207 2104841-0 1990 MK886, a potent and specific leukotriene biosynthesis inhibitor blocks and reverses the membrane association of 5-lipoxygenase in ionophore-challenged leukocytes. MK-886 0-5 arachidonate 5-lipoxygenase Homo sapiens 112-126 2104841-3 1990 3-[1-(p-Chlorobenzyl)-5-(isopropyl)-3-tert-butylthioindol-2-yl]-2, 2- dimethylpropanoic acid (MK886) is a potent and specific inhibitor of leukotriene biosynthesis in vivo and in intact cells, but has no direct effect on 5-lipoxygenase activity in cell-free systems. MK-886 94-99 arachidonate 5-lipoxygenase Homo sapiens 221-235 2104841-4 1990 In this report, we show that MK886 can both prevent and reverse the membrane translocation of 5-lipoxygenase, in conjunction with the inhibition of leukotriene synthesis. MK-886 29-34 arachidonate 5-lipoxygenase Homo sapiens 94-108 2104841-7 1990 Attempts to demonstrate the effects of MK886 on the association of 5-lipoxygenase with membrane in cell-free preparations failed due to a nonspecific Ca2+-dependent sedimentation of the enzyme. MK-886 39-44 arachidonate 5-lipoxygenase Homo sapiens 67-81 2104841-8 1990 The mechanism of action of MK-886 is therefore to block translocation, prevent subsequent activation of 5-lipoxygenase, and hence block cellular leukotriene biosynthesis. MK-886 27-33 arachidonate 5-lipoxygenase Homo sapiens 104-118 22654897-4 2012 Additionally, significant suppression of the PPARalpha activation by means of MK886 treatment is assumed to provide a new method of treating this deficiency. MK-886 78-83 peroxisome proliferator activated receptor alpha Homo sapiens 45-54 34425199-8 2021 In addition, these effects could be inhibited after treatment with autophagy inhibitor 3-methyladenine (3-MA) and PPARalpha inhibitor MK-886. MK-886 134-140 peroxisome proliferator activated receptor alpha Mus musculus 114-123 34468256-5 2021 RESULTS: We showed that OVA-challenged mice treated with MK-886 or MK-571 had a decrease in inflammatory cells, goblet cells hyperplasia, and eosinophil peroxidase (EPO) activity in the airway. MK-886 57-63 eosinophil peroxidase Mus musculus 142-163 34468256-5 2021 RESULTS: We showed that OVA-challenged mice treated with MK-886 or MK-571 had a decrease in inflammatory cells, goblet cells hyperplasia, and eosinophil peroxidase (EPO) activity in the airway. MK-886 57-63 eosinophil peroxidase Mus musculus 165-168 34432787-9 2021 Incubation of 5d MP with the PPARalpha nuclear receptor antagonist MK-886 or with the nuclear receptor LXR agonist TO-901317 resulted in cancellation of the stimulating effect of adiponectin on apoA-1 gene expression. MK-886 67-73 adiponectin, C1Q and collagen domain containing Homo sapiens 179-190 34396611-8 2021 Interestingly, PPARalpha antagonist MK-886 (30 mg/kg; i.p.) MK-886 36-42 peroxisome proliferator activated receptor alpha Homo sapiens 15-24 34432787-9 2021 Incubation of 5d MP with the PPARalpha nuclear receptor antagonist MK-886 or with the nuclear receptor LXR agonist TO-901317 resulted in cancellation of the stimulating effect of adiponectin on apoA-1 gene expression. MK-886 67-73 apolipoprotein A1 Homo sapiens 194-200 34104311-7 2021 In addition, the administration of specific antagonists of either PPARalpha (MK886) or PPARgamma (GW9662) can effectively decrease the protective effect of PGC-1alpha against hepatic I/R and hepatocyte A/R injuries. MK-886 77-82 peroxisome proliferator activated receptor alpha Homo sapiens 66-75 34104311-7 2021 In addition, the administration of specific antagonists of either PPARalpha (MK886) or PPARgamma (GW9662) can effectively decrease the protective effect of PGC-1alpha against hepatic I/R and hepatocyte A/R injuries. MK-886 77-82 PPARG coactivator 1 alpha Homo sapiens 156-166 32846824-8 2020 However, Angptl4 knock-down with small interfering RNA (siRNA) interference and PPAR-alpha inhibitor MK886 partially abrogated these beneficial effects of TXL. MK-886 101-106 peroxisome proliferator activated receptor alpha Homo sapiens 80-90 32881774-5 2020 In addition, PPARalpha antagonist MK886 or PPARgamma antagonist T0070907 partially eliminated the effect of N15. MK-886 34-39 peroxisome proliferator activated receptor alpha Mus musculus 13-22 32846824-9 2020 Western blotting also revealed that similar with insulin, TXL upregulated the expression of Angptl4 in HCMECs, which could be inhibited by Angptl4 siRNA or MK886 exposure. MK-886 156-161 angiopoietin like 4 Homo sapiens 92-99 32846824-10 2020 TXL treatment increased PPAR-alpha activity, which could be diminished by MK886 but not by Angptl4 siRNA. MK-886 74-79 peroxisome proliferator activated receptor alpha Homo sapiens 24-34 31010302-5 2019 Mechanistically, sh-PPARgamma-mediated phenotypic transformation of VSMCs was partially suppressed by MK886, an antagonist of FLAP. MK-886 102-107 peroxisome proliferator-activated receptor gamma Rattus norvegicus 20-29 32385743-2 2020 RESULTS: The mRNA expression of PPARalpha was significantly induced in HCT116 cells following treatment with chrysin for 36 h, but the mRNA expression of PPARalpha was inhibited, when the cells were treated with a combination of chrysin and MK886 (PPARalpha inhibitor). MK-886 241-246 peroxisome proliferator activated receptor alpha Homo sapiens 32-41 32385743-2 2020 RESULTS: The mRNA expression of PPARalpha was significantly induced in HCT116 cells following treatment with chrysin for 36 h, but the mRNA expression of PPARalpha was inhibited, when the cells were treated with a combination of chrysin and MK886 (PPARalpha inhibitor). MK-886 241-246 peroxisome proliferator activated receptor alpha Homo sapiens 154-163 32385743-2 2020 RESULTS: The mRNA expression of PPARalpha was significantly induced in HCT116 cells following treatment with chrysin for 36 h, but the mRNA expression of PPARalpha was inhibited, when the cells were treated with a combination of chrysin and MK886 (PPARalpha inhibitor). MK-886 241-246 peroxisome proliferator activated receptor alpha Homo sapiens 154-163 32385743-3 2020 This phenomenon proved that the incorporation of MK886 lowers the expression levels of PPARalpha, thus enabling us to study the function of PPARalpha. MK-886 49-54 peroxisome proliferator activated receptor alpha Homo sapiens 87-96 32385743-3 2020 This phenomenon proved that the incorporation of MK886 lowers the expression levels of PPARalpha, thus enabling us to study the function of PPARalpha. MK-886 49-54 peroxisome proliferator activated receptor alpha Homo sapiens 140-149 32385743-8 2020 Comparison of the CYP2S1 and CYP1B1 mRNA expression in chrysin only treated, and a combination of chrysin and MK886-treated HCT116 cells for 24 and 36 h showed a significant difference in the expression levels, indicating that PPARalpha inhibitor could also modify the expression of CYP2S1 and CYP1B1. MK-886 110-115 peroxisome proliferator activated receptor alpha Homo sapiens 227-236 32385743-8 2020 Comparison of the CYP2S1 and CYP1B1 mRNA expression in chrysin only treated, and a combination of chrysin and MK886-treated HCT116 cells for 24 and 36 h showed a significant difference in the expression levels, indicating that PPARalpha inhibitor could also modify the expression of CYP2S1 and CYP1B1. MK-886 110-115 cytochrome P450 family 2 subfamily S member 1 Homo sapiens 283-289 32385743-8 2020 Comparison of the CYP2S1 and CYP1B1 mRNA expression in chrysin only treated, and a combination of chrysin and MK886-treated HCT116 cells for 24 and 36 h showed a significant difference in the expression levels, indicating that PPARalpha inhibitor could also modify the expression of CYP2S1 and CYP1B1. MK-886 110-115 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 294-300 30814036-12 2019 By adding mPGES-1 inhibitor MK886 the abnormal expression and damaged cell function were reversed. MK-886 28-33 prostaglandin E synthase Mus musculus 10-17 31897571-8 2020 reduces conditioned gaping and administration of MK886 (a peroxisome proliferator-activated receptor alpha [PPARalpha] antagonist) blocked THCA"s anti-nausea effect. MK-886 49-54 peroxisome proliferator activated receptor alpha Rattus norvegicus 58-106 31897571-8 2020 reduces conditioned gaping and administration of MK886 (a peroxisome proliferator-activated receptor alpha [PPARalpha] antagonist) blocked THCA"s anti-nausea effect. MK-886 49-54 peroxisome proliferator activated receptor alpha Rattus norvegicus 108-117 31963528-6 2020 MK-886, a PPARalpha antagonist, abrogated the OCT-2 upregulation by metformin and reduced MATE-1 expression. MK-886 0-6 peroxisome proliferator activated receptor alpha Mus musculus 10-19 31963528-6 2020 MK-886, a PPARalpha antagonist, abrogated the OCT-2 upregulation by metformin and reduced MATE-1 expression. MK-886 0-6 POU domain, class 2, transcription factor 2 Mus musculus 46-51 31963528-6 2020 MK-886, a PPARalpha antagonist, abrogated the OCT-2 upregulation by metformin and reduced MATE-1 expression. MK-886 0-6 solute carrier family 47, member 1 Mus musculus 90-96 31010302-5 2019 Mechanistically, sh-PPARgamma-mediated phenotypic transformation of VSMCs was partially suppressed by MK886, an antagonist of FLAP. MK-886 102-107 arachidonate 5-lipoxygenase activating protein Rattus norvegicus 126-130 31466760-10 2019 However, a full LPS-induced fever was observed in tolerant rats pretreated with MK-886, which was associated with an enhancement in the hypothalamic PGE2 levels, that were not accompanied by plasma cytokines (IL-1beta, and IL-6) and PGE2 surges. MK-886 80-86 interleukin 6 Rattus norvegicus 223-227 31063807-6 2019 Moreover, F215 also markedly alleviated osteoarthritic pain in rats, and the therapeutic effects of F215 were blocked by the PPAR-alpha antagonist MK886. MK-886 147-152 peroxisome proliferator activated receptor alpha Rattus norvegicus 125-135 31379583-6 2019 The pharmacological effects of carmofur were partially blocked by peroxisome proliferator-activated receptor-alpha (PPARalpha) antagonist MK886 and cannabinoid receptor 2 (CB2) antagonist SR144528, indicating that carmofur attenuated LPS-induced ALI in a PPARalpha- and CB2-dependent mechanism. MK-886 138-143 peroxisome proliferator activated receptor alpha Mus musculus 116-125 30635472-8 2019 However, the aforementioned effects of PEA were completely or partially abolished by MK886, a selective PPARalpha antagonist. MK-886 85-90 peroxisome proliferator activated receptor alpha Rattus norvegicus 104-113 30819230-13 2019 Finally, TRPM7 silencing attenuated the PI3K/AKT activation, which was enhanced by BAPTA-AM, MK886 or LY2904002 treatment in ovarian cancer cells. MK-886 93-98 transient receptor potential cation channel subfamily M member 7 Homo sapiens 9-14 30819230-13 2019 Finally, TRPM7 silencing attenuated the PI3K/AKT activation, which was enhanced by BAPTA-AM, MK886 or LY2904002 treatment in ovarian cancer cells. MK-886 93-98 AKT serine/threonine kinase 1 Homo sapiens 45-48 30819230-10 2019 Similar to that of TRPM7 silencing, treatment with MK886, a potent 5-lipoxygenase inhibitor to reduce TRPM7 expression, and/or BAPTA-AM, an intracellular calcium chelator, significantly mitigated the Epidermal growth factor (EGF) or Insulin-like growth factors (IGF)-stimulated migration, invasion, and the EMT in ovarian cancer cells by decreasing the levels of intracellular calcium [Ca2+]i. MK-886 51-56 arachidonate 5-lipoxygenase Homo sapiens 67-81 30819230-10 2019 Similar to that of TRPM7 silencing, treatment with MK886, a potent 5-lipoxygenase inhibitor to reduce TRPM7 expression, and/or BAPTA-AM, an intracellular calcium chelator, significantly mitigated the Epidermal growth factor (EGF) or Insulin-like growth factors (IGF)-stimulated migration, invasion, and the EMT in ovarian cancer cells by decreasing the levels of intracellular calcium [Ca2+]i. MK-886 51-56 transient receptor potential cation channel subfamily M member 7 Homo sapiens 102-107 30557558-7 2019 On the other hand, in isolated CD4+ T cells from experimental autoimmune myocarditis (EAM) rats, PPARalpha agonist Fenofibrate decreased the expression of IL-17 and RORgammat, increased the expression of Foxp3, while PPARalpha antagonist MK886 reversed these effects. MK-886 238-243 peroxisome proliferator activated receptor alpha Rattus norvegicus 97-106 30551401-9 2019 Meanwhile, MK886, a PPARalpha antagonist, GSK0660, a PPARbeta antagonist, and GW9662, a PPARgamma antagonist, reversed the protection of naringenin on cardiomyocytes (P < 0.05), and abrogated the up-regulation of CYP2J3-EET produced by naringenin (P < 0.05). MK-886 11-16 peroxisome proliferator activated receptor alpha Rattus norvegicus 20-29 30192835-9 2018 In contrast, inhibition of LOX with MK886, thus reduction of leukotriene formation during chronic enteritis, did not affect the inhibition of B0AT1. MK-886 36-41 polyunsaturated fatty acid lipoxygenase ALOX15 Oryctolagus cuniculus 27-30 29912977-7 2018 However, Angptl4 knock-down with siRNA interference and inhibition of PPAR-alpha with MK886 partially diminished these beneficial effects of TXL and rhAngptl4. MK-886 86-91 peroxisome proliferator activated receptor alpha Homo sapiens 70-80 28236037-6 2018 However, these effects of osthole were reduced or abrogated after simultaneous addition of the specific PPARalpha antagonist MK886 or/and the PPARgamma antagonist GW9662, especially in the co-PPARalpha/gamma antagonists-treated group. MK-886 125-130 peroxisome proliferator activated receptor alpha Rattus norvegicus 104-113 30931090-10 2019 Furthermore, 4g showed high anti-inflammatory activities in lipopolysaccharide (LPS) induced acute lung injury (ALI) model, and this effect was blocked by pre-treatment with the PPAR-alpha antagonist MK886. MK-886 200-205 peroxisome proliferator activated receptor alpha Homo sapiens 178-188 30658033-7 2018 In cultured corneal epithelial sheets, qRT-PCR, WB, and SEM determined the individual effects of fenofibrate and MK886 (PPARalpha agonist and antagonist, respectively) on PPARalpha, TRPV6 expression, and SCEC microvilli morphology. MK-886 113-118 transient receptor potential cation channel, subfamily V, member 6 Mus musculus 182-187 29936999-10 2018 In addition, rats undergoing T/HS were treated with MK-886, a known ALOX5AP inhibitor. MK-886 52-58 arachidonate 5-lipoxygenase activating protein Rattus norvegicus 68-75 29936999-13 2018 ALOX5/ALOX5AP complex formation, leukotriene production, and lung injury were decreased after inhibition of ALOX5AP with MK-886. MK-886 121-127 arachidonate 5-lipoxygenase Rattus norvegicus 0-5 29936999-13 2018 ALOX5/ALOX5AP complex formation, leukotriene production, and lung injury were decreased after inhibition of ALOX5AP with MK-886. MK-886 121-127 arachidonate 5-lipoxygenase activating protein Rattus norvegicus 6-13 29936999-13 2018 ALOX5/ALOX5AP complex formation, leukotriene production, and lung injury were decreased after inhibition of ALOX5AP with MK-886. MK-886 121-127 arachidonate 5-lipoxygenase activating protein Rattus norvegicus 108-115 29777706-4 2018 Additionally, MK 886 was used to inhibit PPAR-alpha. MK-886 14-20 peroxisome proliferator activated receptor alpha Mus musculus 41-51 28784429-4 2018 The early development of FLAP inhibitors (i.e. MK-886, MK-591, BAY-X-1005) mostly concentrated on asthma cure, and resulted in promising readouts in preclinical and clinical studies with asthma patients. MK-886 47-53 arachidonate 5-lipoxygenase activating protein Homo sapiens 25-29 29271063-10 2018 However, inhibition of lipoxygenase (LOX) with MK886, thus reducing leukotriene formation during chronic enteritis, reversed the stimulation of SN2. MK-886 47-52 polyunsaturated fatty acid lipoxygenase ALOX15 Oryctolagus cuniculus 23-35 29271063-10 2018 However, inhibition of lipoxygenase (LOX) with MK886, thus reducing leukotriene formation during chronic enteritis, reversed the stimulation of SN2. MK-886 47-52 polyunsaturated fatty acid lipoxygenase ALOX15 Oryctolagus cuniculus 37-40 29271063-10 2018 However, inhibition of lipoxygenase (LOX) with MK886, thus reducing leukotriene formation during chronic enteritis, reversed the stimulation of SN2. MK-886 47-52 sodium-coupled neutral amino acid transporter 5 Oryctolagus cuniculus 144-147 29080294-8 2018 The in vitro and in vivo effects of MPsPPARalpha+/+ were abolished in presence of MK886, a specific inhibitor of PPARalpha. MK-886 82-87 peroxisome proliferator activated receptor alpha Mus musculus 39-48 28736035-15 2017 Furthermore, the PPARalpha antagonist MK886 or PPARgamma antagonist T0070907 respectively partly abolished the anti-inflammatory effects of N15 in vitro. MK-886 38-43 peroxisome proliferator activated receptor alpha Mus musculus 17-26 28737505-5 2017 Lower doses of the FLAP inhibitor MK886 were required to reduce LTB4 levels in exudates of female versus male mice and rats. MK-886 34-39 arachidonate 5-lipoxygenase activating protein Mus musculus 19-23