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1 olyunsaturated n-6 fatty acid) by the enzyme 5-lipoxygenase.
2 sing pharmacologic and genetic abrogation of 5-lipoxygenase.
3 a novel import sequence at Arg(518) on human 5-lipoxygenase.
4 ability of this class of chelator to inhibit 5-lipoxygenase.
5 nhibitor of CoA-independent transacylase and 5-lipoxygenase.
6 leukocytes is rapidly converted to LTA(4) by 5-lipoxygenase.
7 opentenyl hydroxamic acid-based inhibitor of 5-lipoxygenase.
8 scent protein to the same degree as complete 5-lipoxygenase.
9 ated by activation of phospholipase A(2) and 5-lipoxygenase.
10 unchanged, indicating an abnormality beyond 5-lipoxygenase.
11 levels of NF-kappaB, AKT, ERK1/2, COX-2, and 5-lipoxygenase.
12 ctivity of the iron-containing metalloenzyme 5-lipoxygenase.
13 d in the nucleus, where it co-localizes with 5-lipoxygenase.
14 lear ratio of a key SPM biosynthetic enzyme, 5-lipoxygenase.
15 and its conversion to bioactive lipoxins by 5-lipoxygenase.
17 lammatory leukotrienes (LTs) are produced by 5-lipoxygenase (5-LO) aided by 5-LO-activating protein (
18 odel of human asthma to detect lung mRNA for 5-lipoxygenase (5-LO) and 5-LO-activating protein (FLAP)
20 CSC), but they also suppress the activity of 5-lipoxygenase (5-LO) at clinically feasible concentrati
30 e repeat polymorphism in the promoter of the 5-lipoxygenase (5-LO) gene have been associated with car
32 genases (COX), and leukotrienes, produced by 5-lipoxygenase (5-LO) have been implicated in cancer pro
39 al prostaglandin E2 synthase-1 (mPGES-1) and 5-lipoxygenase (5-LO) is currently pursued as potential
45 (cysLTs), are lipid mediators formed by the 5-lipoxygenase (5-LO) pathway of arachidonic acid metabo
50 lthough Alox5 expression and the presence of 5-lipoxygenase (5-LO) protein in BMDMs was observed, the
53 inflammatory mediator produced by the enzyme 5-lipoxygenase (5-LO), is associated with the developmen
54 ying prostaglandin E2 synthase (mPGES)-1 and 5-lipoxygenase (5-LO), key enzymes linking inflammation
55 s of cytosolic phospholipase A(2) (cPLA(2)), 5-lipoxygenase (5-LO), or 5-LO activating protein (FLAP)
56 lipid mediator of inflammation formed by the 5-lipoxygenase (5-LO)-catalyzed oxidation of arachidonic
57 Although overproduction of proinflammatory 5-lipoxygenase (5-LO)-derived leukotrienes (LTs) has bee
59 oid biosynthesis from predominantly LTB4 and 5-lipoxygenase (5-LO)-initiated pathways to LXA4, a 15-L
63 ortant to both airway remodeling [TGF-beta1, 5-lipoxygenase (5-LO)] and airway-hyperresponsiveness (A
64 roducts of the biosynthetic crossover of the 5-lipoxygenase (5-LOX) and cyclooxygenase-2 (COX-2) path
73 donic acid in a 2-step reaction catalyzed by 5-lipoxygenase (5-LOX) requiring the formation of 5-HPET
74 alpha-demethylase (CYP51 or Erg11) and human 5-lipoxygenase (5-LOX) with improved potency against 5-L
75 MK-886, a functional inhibitor of the enzyme 5-lipoxygenase (5-LOX), and found increased GluR1 phosph
78 T biosynthesis is initiated by the action of 5-lipoxygenase (5-LOX), which catalyzes the transformati
83 hieved through intracellular localization of 5-lipoxygenase (5-LOX): nuclear 5-LOX favors the biosynt
84 1beta (IL-1alpha/beta(-/-)) or leukotrienes (5-lipoxygenase [5-LOX(-/-)]) produced arthritis of inter
85 ays (cyclooxygenase-2 [COX-2], celecoxib and 5-lipoxygenase [5-LOX], zileuton) added to chemotherapy
87 mediators of inflammation (cyclooxygenase 2, 5-lipoxygenase, 5-lipoxygenase-activating protein, tumor
90 T/Ei) F(2) cross and identified arachidonate 5-lipoxygenase (5LO) as a candidate gene in this region.
92 transcellular biosynthesis: cells expressing 5-lipoxygenase (5LO) form LTA(4) and transfer it to cell
93 nt role for leukotriene (LT) biosynthesis by 5-lipoxygenase (5LO) in the impairment of HPV by endotox
95 provide in vitro experimental evidence that 5-Lipoxygenase (5LO) is as an endogenous regulator for G
98 arcinogenesis, but the role of hematopoietic 5-lipoxygenase (5LO) that may impact tumor immunity in d
101 stress up-regulates the ALOX5 gene product, 5-lipoxygenase (5LO), herein we investigated its role in
105 A drug discovery program in search of novel 5-lipoxygenase activating protein (FLAP) inhibitors focu
107 diovascular disease, and an inhibitor of the 5-lipoxygenase activating protein (FLAP) is in clinical
109 s showed hypoxia augmented the expression of 5-lipoxygenase activating protein (FLAP), a key enzyme i
110 e show that expression of 5-lipoxygenase and 5-lipoxygenase activating protein (FLAP), key catalytic
113 ave previously reported that exposure to the 5-lipoxygenase activating protein-directed inhibitor MK8
114 genase (ALOX5) and its partner, arachidonate 5-lipoxygenase-activating protein (ALOX5AP), are involve
115 derivative 11j has an IC(50) of 4.2 nM in a 5-lipoxygenase-activating protein (FLAP) binding assay,
116 ed the mRNA expression of 5-lipoxygenase and 5-lipoxygenase-activating protein (FLAP) in human pulmon
117 n of a novel series of oxadiazole-containing 5-lipoxygenase-activating protein (FLAP) inhibitors are
118 y proteins, coactosin-like protein (CLP) and 5-lipoxygenase-activating protein (FLAP), can support 5L
119 ere it associates with its scaffold protein, 5-lipoxygenase-activating protein (FLAP), to form the co
120 ctions in this model were examined using the 5-lipoxygenase-activating protein inhibitor MK-886.
124 diaI infarction, including ALOX5AP (encoding 5-lipoxygenase-activating protein) associated with myoca
125 as serine proteinases, histamine 4-receptor, 5-lipoxygenase-activating protein, 15-lipoxygenase-1, pr
126 o-localizes with cPLA2alpha, 5-lipoxygenase, 5-lipoxygenase-activating protein, and leukotriene C4 sy
127 or cysLT synthesis by MK886, an inhibitor of 5-lipoxygenase-activating protein, reduced the response
128 lammation (cyclooxygenase 2, 5-lipoxygenase, 5-lipoxygenase-activating protein, tumor necrosis factor
129 re centered on the integral membrane protein 5-Lipoxygenase-Activating Protein, which we identify as
130 physiologically relevant manner with modest 5-lipoxygenase activation and formation of leukotrienes.
131 nvolving p38 and JNK MAPK, cPLA(2)alpha, and 5-lipoxygenase activation and resulting in the amplifica
132 n of soluble EMMPRIN, phospholipase A(2) and 5-lipoxygenase activities are sites for potential therap
133 in AERD may lead to dysregulated control of 5-lipoxygenase activity by PGE(2), whereas adherent plat
137 eated with recombinant adenovirus expressing 5-lipoxygenase (Ad5LO), BMPR2(+/-) mice exhibited signif
138 Genotype at rs1864414 in the arachidonate 5-lipoxygenase ALOX5 was also associated with decreased
139 e leukotriene-generating enzyme arachidonate 5-lipoxygenase (Alox5) abrogates neutrophil pro-metastat
140 from the same pathway, in which arachidonate 5-lipoxygenase (ALOX5) and its partner, arachidonate 5-l
141 of the Sp1-binding motif in the arachidonate 5-lipoxygenase (ALOX5) gene promoter (either 5/5, 5/x, o
144 roid cells, increased the mRNA expression of 5-lipoxygenase and 5-lipoxygenase-activating protein (FL
145 Intravenous anesthetic propofol binds to 5-lipoxygenase and attenuates leukotriene B4 production.
146 e prostanoid mediators cyclo-oxygenase-2 and 5-lipoxygenase and CC chemokine receptor antagonist Met-
147 assay systems, 10 micro m AACOCF3 inhibited 5-lipoxygenase and CoA-independent transacylase activiti
148 antinociceptive effect whereas inhibitors of 5-lipoxygenase and cyclooxygenase augmented the DOR anti
149 potential therapeutic benefits of combining 5-lipoxygenase and cyclooxygenase inhibitors for maximal
150 s subsequently metabolized by the actions of 5-lipoxygenase and cyclooxygenase to form LTC(4) and PGD
152 its leukotriene biosynthesis in concert with 5-lipoxygenase and cytosolic phospholipase A(2)alpha act
157 provide the first direct evidence that host 5-lipoxygenase and lipoxygenase products of arachidonic
160 (ROS) through a Rac1-dependent mechanism via 5-lipoxygenase and the mitochondria, leading to the biph
161 eries of bone marrow chimeras generated from 5-lipoxygenase(-/-) and leukotriene A(4) (LTA(4)) hydrol
162 whereas expression levels of MUC5AC, MUC5B, 5-lipoxygenase, and 15-lipoxygeanse 1 were similar to th
163 quential engagement of Abcb1, SP1 receptors, 5-lipoxygenase, and Abcc1 to enhance T cell migration an
164 er eicosanoid-related enzymes, namely COX-1, 5-lipoxygenase, and cytosolic phospholipase A(2) were no
165 the participation of multidrug transporters, 5-lipoxygenase, and G protein-coupled receptors for chem
168 eries of bone marrow chimeras generated from 5-lipoxygenase- and LTA(4) hydrolase-deficient mice, we
169 the utility of this approach by identifying 5-lipoxygenase as underlying previously identified quant
171 itory action of 47.Na occurs at the stage of 5-lipoxygenase biosynthesis as it blocks both leukotrien
172 ic residues that 1) were common to different 5-lipoxygenases but not shared with other lipoxygenases,
173 tty acids including AA activated cPLA(2) and 5-lipoxygenase by increasing [Ca(2+)](i) and inducing cP
175 evated serum LTB4 and synovial expression of 5-lipoxygenase correlated with increased disease severit
177 indicated that only the N-terminal domain of 5-lipoxygenase could carry out this translocation functi
178 sfer of autoreactive T cells from B6 mice to 5-lipoxygenase-deficient (5-LO-/-) mice, which have a fu
183 al alterations were significantly reduced in 5-lipoxygenase-deficient mice, but not 12/15-lipoxygenas
184 istopathology was significantly inhibited in 5-lipoxygenase-deficient mice, but not in 12/15-lipoxyge
186 fic NADP(+)-dependent dehydrogenase utilizes 5-lipoxygenase-derived 5-hydroxy-6,8,11,14-eicosatetraen
188 redoxin reductase, and the overexpression of 5-lipoxygenase did not inhibit thioredoxin reductase or
191 Ai knockdown or pharmacological block of the 5-lipoxygenase enzyme prevented activated mast cells fro
192 e infection model of GAS in mice lacking the 5-lipoxygenase enzyme to determine the role of endogenou
193 chidonic acid can then be metabolized by the 5-lipoxygenase enzyme to generate the proinflammatory si
199 , we hypothesized that a polymorphism in the 5-lipoxygenase gene promoter could relate to atheroscler
203 and its cytoplasmic targets HSP25/27, LSP-1, 5-lipoxygenase, glycogen synthase, and tyrosine hydroxyl
204 from arachidonic acid through the action of 5-lipoxygenase have been known for over two decades and
205 antagonists of the type 1 cysLT receptor or 5-lipoxygenase, implying that bronchoconstriction and MC
209 e was also found to accumulate together with 5-lipoxygenase in the nucleus of alveolar macrophages.
210 Inhibition of the LTB4 biosynthetic enzyme 5-lipoxygenase inhibited toxin A-induced increases in il
211 a) inhibit synthesis of leukotriene (through 5-lipoxygenase inhibition) or (b) block the cysLT recept
215 bitor, nordihydroguaiaretic acid (NDGA), the 5-lipoxygenase inhibitor, AA861, the epoxygenase inhibit
223 cium-independent phospholipase A2, 12/15 and 5-lipoxygenase) is expressed in mouse submandibular glan
224 ition of endogenous leukotriene synthesis by 5-lipoxygenase knockout in mice or by pharmacologic mean
226 neonatally sensitized mice showed increased 5-lipoxygenase levels, whereas adult mice expressed more
227 A(4), an eicosanoid mediator that depends on 5-lipoxygenase (LO) for its biosynthesis, exerts a regul
229 19-2, we co-expressed in human macrophages a 5-lipoxygenase (LOX) 3'UTR-luciferase reporter vector to
231 Thus, the predicted beta-barrel domain of 5-lipoxygenase may function like the C2 domain within pr
232 hese results indicate that nuclear import of 5-lipoxygenase may reflect the combined functional effec
234 , phosphorylated FTY720, or S1P also require 5-lipoxygenase-mediated synthesis of cysteinyl leukotrie
236 geted gene expression data demonstrated that 5-lipoxygenase metabolites correlated with the pathogeni
237 e results suggest that the concentrations of 5-lipoxygenase metabolites of arachidonic acid, 5-hydrox
240 tes leukotriene synthesis; nuclear import of 5-lipoxygenase modulates leukotriene synthetic capacity.
242 enase-activating protein rescues activity of 5-lipoxygenase mutations that delay nuclear membrane ass
244 way was ineffective, whereas blocking either 5-lipoxygenase of the lipoxygenase pathway or the cycloo
246 lipoxygenase pathway either directly through 5'-lipoxygenase or via antagonism of the leukotriene B4
248 ns of proinflammatory lipid mediators of the 5-lipoxygenase pathway are significantly higher in MIAC
249 triene C(4) synthase (LTC(4)S), the terminal 5-lipoxygenase pathway enzyme that is responsible for th
252 re potent lipid mediators synthesized by the 5-lipoxygenase pathway of arachidonic acid (AA) metaboli
253 The cysteinyl leukotrienes (cys-LTs) are 5-lipoxygenase pathway products implicated in asthma, in
255 east cancer cells produce metabolites of the 5-lipoxygenase pathway such as leukotriene B4 to activat
258 opose that PPARalpha in B cells and/or tumor 5-lipoxygenase pathways represents new targets for pharm
259 B(4) biosynthesis is to activate cPLA(2) and 5-lipoxygenase primarily by liberating from the outer pl
260 n of COX-2-derived prostanoids and augmented 5-lipoxygenase product formation, consistent with COX-2
261 11,14-eicosatetraenoic acid (5-oxo-ETE) is a 5-lipoxygenase product that acts via the selective OXE r
262 11,14-eicosatetraenoic acid (5-oxo-ETE) is a 5-lipoxygenase product that is a potent granulocyte chem
263 derivatives reported here identify specific 5-lipoxygenase products as candidate physiologically rel
265 verall capacity of whole blood to synthesize 5-lipoxygenase products; these genotype-related changes
266 IL-10, suggesting a direct link between the 5-lipoxygenase proinflammatory pathway and IL-10 regulat
270 are generated by cyclooxygenase isozymes and 5-lipoxygenase, respectively, and their biosynthesis and
271 utative bipartite nuclear import sequence of 5-lipoxygenase revealed that this region formed an alpha
272 o and in a murine model of inflammation that 5-lipoxygenase stimulation induces PPAR-alpha signaling
273 arine n-3 fatty acids (including a competing 5-lipoxygenase substrate that reduces the production of
277 ry products of arachidonic acid oxidation by 5-lipoxygenase that have been shown to be involved in re
278 hin the nuclear localization sequence-518 of 5-lipoxygenase, the ability of protein kinase A to phosp
279 enes is tightly regulated, and expression of 5-lipoxygenase, the enzyme required for the first step i
280 marrow cells from nondiabetic mice expressed 5-lipoxygenase, the enzyme required for the initiation o
283 o FLAP and subsequently being transferred to 5-lipoxygenase, thereby preventing leukotriene biosynthe
286 group V sPLA(2) induced the translocation of 5-lipoxygenase to the nuclear envelope at which they wer
287 lux also promotes translocation of cytosolic 5-lipoxygenase to the nuclear membrane, a key step in th
288 include the inhibition of protein kinase C, 5-lipoxygenase, tyrosine-kinase as well as cyclooxygenas
291 n corresponding to residues 518-530 on human 5-lipoxygenase was found to be unique to 5-lipoxygenase
295 vealed that leukotriene A(4) hydrolase, like 5-lipoxygenase, was most abundant in the nucleus, with o
296 as well as cytosolic phospholipase A(2) and 5-lipoxygenase were markedly reduced by SB202190 in unst
299 ulation of two metabolic pathways (cPLA2 and 5-lipoxygenase), which results in the generation of both
300 ngly, two subpopulations of cells expressing 5-lipoxygenase with this mutated region could be discern
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