ライフサイエンスコーパス: 5-lipoxygenase

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 ctivity of the iron-containing metalloenzyme 5-lipoxygenase.

12 d in the nucleus, where it co-localizes with 5-lipoxygenase.

13 levels of NF-kappaB, AKT, ERK1/2, COX-2, and 5-lipoxygenase.

14 lear ratio of a key SPM biosynthetic enzyme, 5-lipoxygenase.

15 and its conversion to bioactive lipoxins by 5-lipoxygenase.

16 Arachidonate-5-lipoxygenase (5-LO) activity and increased leukotriene

17 lammatory leukotrienes (LTs) are produced by 5-lipoxygenase (5-LO) aided by 5-LO-activating protein (

18 tion analysis to observe the organization of 5-lipoxygenase (5-LO) and 5-lipoxygenase-activating prot

19 The enzymes 5-lipoxygenase (5-LO) and glycogen synthase kinase (GSK)

20 CSC), but they also suppress the activity of 5-lipoxygenase (5-LO) at clinically feasible concentrati

21 Mammalian 5-lipoxygenase (5-LO) catalyzes conversion of arachidoni

22 The enzyme 5-lipoxygenase (5-LO) catalyzes the conversion of arachi

23 Mammalian 5-lipoxygenase (5-LO) catalyzes the conversion of arachi

24 5-Lipoxygenase (5-LO) catalyzes the rate-limiting step o

25 ety as novel soluble epoxide hydrolase (sEH)/5-lipoxygenase (5-LO) dual inhibitors.

26 The 5-lipoxygenase (5-LO) enzymatic pathway is widely distri

27 The 5-lipoxygenase (5-LO) enzyme is widely distributed withi

28 To initiate LT formation, the 5-lipoxygenase (5-LO) enzyme translocates to nuclear mem

29 Here we identify the arachidonate 5-lipoxygenase (5-LO) gene (Alox5) as a critical regulat

30 e repeat polymorphism in the promoter of the 5-lipoxygenase (5-LO) gene have been associated with car

31 acid (AA) into prostaglandins (PGs), whereas 5-lipoxygenase (5-LO) generates leukotrienes (LT).

32 genases (COX), and leukotrienes, produced by 5-lipoxygenase (5-LO) have been implicated in cancer pro

33 lloenzymes ribonucleotide reductase (RR) and 5-lipoxygenase (5-LO) have been investigated.

34 with the leukotriene (LT)-initiating enzyme 5-lipoxygenase (5-LO) in the MC nucleus.

35 The enzyme 5-lipoxygenase (5-LO) initiates the biosynthesis of leuk

36 The enzyme 5-lipoxygenase (5-LO) initiates the synthesis of leukotr

37 The activation of 5-lipoxygenase (5-LO) involves its calcium-dependent tra

38 5-Lipoxygenase (5-LO) is a protein widely distributed in

39 al prostaglandin E2 synthase-1 (mPGES-1) and 5-lipoxygenase (5-LO) is currently pursued as potential

40 The enzyme 5-lipoxygenase (5-LO) is key in the synthesis of leukotr

41 5-Lipoxygenase (5-LO) is the key enzyme in leukotriene b

42 5-Lipoxygenase (5-LO) is the rate-limiting enzyme in leu

43 Lipid mediators derived from 5-lipoxygenase (5-LO) metabolism can activate both pro-

44 ost developed compounds primarily target the 5-lipoxygenase (5-LO) or the cyclooxygenase (COX) pathwa

45 Activation of the 5-lipoxygenase (5-LO) pathway leads to the biosynthesis

46 (cysLTs), are lipid mediators formed by the 5-lipoxygenase (5-LO) pathway of arachidonic acid metabo

47 We hypothesized that the 5-lipoxygenase (5-LO) pathway of LT metabolism plays an

48 To evaluate the role of the 5-lipoxygenase (5-LO) pathway on breast cancer growth re

49 LTs, the products of the 5-lipoxygenase (5-LO) pathway, are potent lipid mediator

50 proinflammatory cyclooxygenase-2 (COX-2) and 5-lipoxygenase (5-LO) pathways and concurrently reduces

51 In contrast, 5-lipoxygenase (5-LO) produces the generally proinflamma

52 lthough Alox5 expression and the presence of 5-lipoxygenase (5-LO) protein in BMDMs was observed, the

53 5-Lipoxygenase (5-LO) was the primary enzyme involved in

54 Mice that are deficient for the enzyme 5-lipoxygenase (5-LO), and therefore lack LTs, exhibit a

55 inflammatory mediator produced by the enzyme 5-lipoxygenase (5-LO), is associated with the developmen

56 ying prostaglandin E2 synthase (mPGES)-1 and 5-lipoxygenase (5-LO), key enzymes linking inflammation

57 s of cytosolic phospholipase A(2) (cPLA(2)), 5-lipoxygenase (5-LO), or 5-LO activating protein (FLAP)

58 5-Lipoxygenase (5-LO)-activating protein (FLAP) inhibito

59 lipid mediator of inflammation formed by the 5-lipoxygenase (5-LO)-catalyzed oxidation of arachidonic

60 Although overproduction of proinflammatory 5-lipoxygenase (5-LO)-derived leukotrienes (LTs) has bee

61 The 5-lipoxygenase (5-LO)-derived leukotrienes (LTs) influen

62 oid biosynthesis from predominantly LTB4 and 5-lipoxygenase (5-LO)-initiated pathways to LXA4, a 15-L

63 sensitized and challenged mice deficient in 5-lipoxygenase (5-LO).

64 arachidonic acid is initiated by the enzyme 5-lipoxygenase (5-LO).

65 ortant to both airway remodeling [TGF-beta1, 5-lipoxygenase (5-LO)] and airway-hyperresponsiveness (A

66 roducts of the biosynthetic crossover of the 5-lipoxygenase (5-LOX) and cyclooxygenase-2 (COX-2) path

67 Merging of 5-lipoxygenase (5-LOX) and soluble epoxide hydrolase (sE

68 Cyclooxygenase-2 (COX-2) and 5-lipoxygenase (5-LOX) enzymes are overexpressed during

69 This study shows up-regulation of 5-lipoxygenase (5-LOX) in all grades of human PanINs and

70 Potential pro-inflammatory 5-lipoxygenase (5-LOX) inhibition potential (IC50 0.76-0

71 The enzyme 5-lipoxygenase (5-LOX) initiates biosynthesis of the pro

72 of pharmacological and genetic inhibition of 5-lipoxygenase (5-Lox) on cell proliferation, apoptosis

73 s oxidized to proinflammatory eicosanoids by 5-lipoxygenase (5-LOX) on the nuclear envelope.

74 The 5-lipoxygenase (5-LOX) pathway is critical for pancreati

75 pecifically the cyclooxygenase-2 (COX-2) and 5-lipoxygenase (5-LOX) pathways, participate in the indu

76 r inhibitors of the cyclooxygenase (COX) and 5-lipoxygenase (5-LOX) pathways.

77 We reported earlier that arachidonate 5-lipoxygenase (5-Lox) plays an important role in the su

78 donic acid in a 2-step reaction catalyzed by 5-lipoxygenase (5-LOX) requiring the formation of 5-HPET

79 alpha-demethylase (CYP51 or Erg11) and human 5-lipoxygenase (5-LOX) with improved potency against 5-L

80 MK-886, a functional inhibitor of the enzyme 5-lipoxygenase (5-LOX), and found increased GluR1 phosph

81 CNB-001 is a potent inhibitor of 5-lipoxygenase (5-LOX), decreases 5-LOX expression, and

82 c acid by either cyclooxygenase-2 (COX-2) or 5-lipoxygenase (5-LOX), respectively.

83 T biosynthesis is initiated by the action of 5-lipoxygenase (5-LOX), which catalyzes the transformati

84 Leukotrienes generated by 5-lipoxygenase (5-LOX)-catalyzed reaction are key regula

85 Propofol attenuated the production of 5-lipoxygenase (5-LOX)-related arachidonic acid (AA) der

86 ti-inflammatory lipoxins requires the enzyme 5-lipoxygenase (5-LOX).

87 4)) in two successive reactions catalyzed by 5-lipoxygenase (5-LOX).

88 hieved through intracellular localization of 5-lipoxygenase (5-LOX): nuclear 5-LOX favors the biosynt

89 1beta (IL-1alpha/beta(-/-)) or leukotrienes (5-lipoxygenase [5-LOX(-/-)]) produced arthritis of inter

90 ays (cyclooxygenase-2 [COX-2], celecoxib and 5-lipoxygenase [5-LOX], zileuton) added to chemotherapy

91 There it co-localizes with cPLA2alpha, 5-lipoxygenase, 5-lipoxygenase-activating protein, and l

92 mediators of inflammation (cyclooxygenase 2, 5-lipoxygenase, 5-lipoxygenase-activating protein, tumor

93 We previously reported that the enzyme 5-Lipoxygenase (5LO) acts as a modulator of Abeta peptid

94 Here, we evaluated the role of 5-lipoxygenase (5LO) and its chemotactic metabolite leuk

95 T/Ei) F(2) cross and identified arachidonate 5-lipoxygenase (5LO) as a candidate gene in this region.

96 The 5-lipoxygenase (5LO) enzyme is upregulated in Alzheimer

97 transcellular biosynthesis: cells expressing 5-lipoxygenase (5LO) form LTA(4) and transfer it to cell

98 nt role for leukotriene (LT) biosynthesis by 5-lipoxygenase (5LO) in the impairment of HPV by endotox

99 5-Lipoxygenase (5LO) is a key enzyme in leukotriene (LT)

100 provide in vitro experimental evidence that 5-Lipoxygenase (5LO) is as an endogenous regulator for G

101 5-Lipoxygenase (5LO) is upregulated in Alzheimer's disea

102 The 5-lipoxygenase (5LO) produces leukotriene B(4) and 15-ep

103 arcinogenesis, but the role of hematopoietic 5-lipoxygenase (5LO) that may impact tumor immunity in d

104 5-Lipoxygenase (5LO) was recently identified as a gene t

105 5-Lipoxygenase (5LO), by producing leukotrienes, is a pr

106 stress up-regulates the ALOX5 gene product, 5-lipoxygenase (5LO), herein we investigated its role in

107 Use of T cells deficient in 5-lipoxygenase, Abcb1, and Abcc1, and comparison of the

108 mic stroke: phosphodiesterase 4D (PDE4D) and 5-lipoxygenase activating protein (ALOX5AP).

109 Although deletion of the 5-lipoxygenase activating protein (FLAP) did not influen

110 5-Lipoxygenase activating protein (FLAP) inhibitors atte

111 A drug discovery program in search of novel 5-lipoxygenase activating protein (FLAP) inhibitors focu

112 5-lipoxygenase activating protein (FLAP) is abundantly p

113 diovascular disease, and an inhibitor of the 5-lipoxygenase activating protein (FLAP) is in clinical

114 5-Lipoxygenase activating protein (FLAP) plays a critica

115 s showed hypoxia augmented the expression of 5-lipoxygenase activating protein (FLAP), a key enzyme i

116 e show that expression of 5-lipoxygenase and 5-lipoxygenase activating protein (FLAP), key catalytic

117 We examined expression of the 5-lipoxygenase activating protein (FLAP), which is criti

118 ists of multimers of LTC(4) synthase and the 5-lipoxygenase activating protein (FLAP).

119 ave previously reported that exposure to the 5-lipoxygenase activating protein-directed inhibitor MK8

120 genase (ALOX5) and its partner, arachidonate 5-lipoxygenase-activating protein (ALOX5AP), are involve

121 derivative 11j has an IC(50) of 4.2 nM in a 5-lipoxygenase-activating protein (FLAP) binding assay,

122 ed the mRNA expression of 5-lipoxygenase and 5-lipoxygenase-activating protein (FLAP) in human pulmon

123 n of a novel series of oxadiazole-containing 5-lipoxygenase-activating protein (FLAP) inhibitors are

124 he organization of 5-lipoxygenase (5-LO) and 5-lipoxygenase-activating protein (FLAP) into higher ord

125 y proteins, coactosin-like protein (CLP) and 5-lipoxygenase-activating protein (FLAP), can support 5L

126 ere it associates with its scaffold protein, 5-lipoxygenase-activating protein (FLAP), to form the co

127 GSK2190915, a potent 5-lipoxygenase-activating protein inhibitor, prevents th

128 The potent and selective 5-lipoxygenase-activating protein leukotriene synthesis

129 5-Lipoxygenase-activating protein rescues activity of 5-

130 diaI infarction, including ALOX5AP (encoding 5-lipoxygenase-activating protein) associated with myoca

131 as serine proteinases, histamine 4-receptor, 5-lipoxygenase-activating protein, 15-lipoxygenase-1, pr

132 o-localizes with cPLA2alpha, 5-lipoxygenase, 5-lipoxygenase-activating protein, and leukotriene C4 sy

133 or cysLT synthesis by MK886, an inhibitor of 5-lipoxygenase-activating protein, reduced the response

134 lammation (cyclooxygenase 2, 5-lipoxygenase, 5-lipoxygenase-activating protein, tumor necrosis factor

135 re centered on the integral membrane protein 5-Lipoxygenase-Activating Protein, which we identify as

136 physiologically relevant manner with modest 5-lipoxygenase activation and formation of leukotrienes.

137 nvolving p38 and JNK MAPK, cPLA(2)alpha, and 5-lipoxygenase activation and resulting in the amplifica

138 n of soluble EMMPRIN, phospholipase A(2) and 5-lipoxygenase activities are sites for potential therap

139 in AERD may lead to dysregulated control of 5-lipoxygenase activity by PGE(2), whereas adherent plat

140 immunoreactive LTC(4)S protein expression or 5-lipoxygenase activity.

141 g transporters, Abcb1 and Abcc1, and through 5-lipoxygenase activity.

142 he nuclear membrane and a 2-fold increase in 5-lipoxygenase activity.

143 eated with recombinant adenovirus expressing 5-lipoxygenase (Ad5LO), BMPR2(+/-) mice exhibited signif

144 Genotype at rs1864414 in the arachidonate 5-lipoxygenase ALOX5 was also associated with decreased

145 e leukotriene-generating enzyme arachidonate 5-lipoxygenase (Alox5) abrogates neutrophil pro-metastat

146 from the same pathway, in which arachidonate 5-lipoxygenase (ALOX5) and its partner, arachidonate 5-l

147 ious HIV-X4 remarkably increase arachidonate 5-lipoxygenase (ALOX5) expression.

148 of the Sp1-binding motif in the arachidonate 5-lipoxygenase (ALOX5) gene promoter (either 5/5, 5/x, o

149 d leukocytes through dual oxidase (Duox) and 5-lipoxygenase (Alox5a).

150 Silencing of lipoxygenase pathways (5-lipoxygenase and 12/15-lipoxygenase), which are import

151 We show that expression of 5-lipoxygenase and 5-lipoxygenase activating protein (FL

152 roid cells, increased the mRNA expression of 5-lipoxygenase and 5-lipoxygenase-activating protein (FL

153 Intravenous anesthetic propofol binds to 5-lipoxygenase and attenuates leukotriene B4 production.

154 e prostanoid mediators cyclo-oxygenase-2 and 5-lipoxygenase and CC chemokine receptor antagonist Met-

155 assay systems, 10 micro m AACOCF3 inhibited 5-lipoxygenase and CoA-independent transacylase activiti

156 antinociceptive effect whereas inhibitors of 5-lipoxygenase and cyclooxygenase augmented the DOR anti

157 potential therapeutic benefits of combining 5-lipoxygenase and cyclooxygenase inhibitors for maximal

158 s subsequently metabolized by the actions of 5-lipoxygenase and cyclooxygenase to form LTC(4) and PGD

159 Roles of 5-lipoxygenase and cyclooxygenase-2 in the biosynthesis

160 its leukotriene biosynthesis in concert with 5-lipoxygenase and cytosolic phospholipase A(2)alpha act

161 It is known that 5-lipoxygenase and its product, leukotriene B4 (LTB4), a

162 tory lipid mediator generated by the enzymes 5-lipoxygenase and leukotriene A(4) hydrolase.

163 quires the sequential action of two enzymes: 5-lipoxygenase and leukotriene A(4) hydrolase.

164 -13 and the leukotriene-synthesizing enzymes 5-lipoxygenase and leukotriene-C4-synthase.

165 provide the first direct evidence that host 5-lipoxygenase and lipoxygenase products of arachidonic

166 man 5-lipoxygenase was found to be unique to 5-lipoxygenase and on a random coil.

167 ed NF-kappaB signaling, and miR-219 targeted 5-lipoxygenase and reduced leukotriene production.

168 (ROS) through a Rac1-dependent mechanism via 5-lipoxygenase and the mitochondria, leading to the biph

169 eries of bone marrow chimeras generated from 5-lipoxygenase(-/-) and leukotriene A(4) (LTA(4)) hydrol

170 whereas expression levels of MUC5AC, MUC5B, 5-lipoxygenase, and 15-lipoxygeanse 1 were similar to th

171 quential engagement of Abcb1, SP1 receptors, 5-lipoxygenase, and Abcc1 to enhance T cell migration an

172 er eicosanoid-related enzymes, namely COX-1, 5-lipoxygenase, and cytosolic phospholipase A(2) were no

173 the participation of multidrug transporters, 5-lipoxygenase, and G protein-coupled receptors for chem

174 Expression of COX-2, 5-lipoxygenase, and p-5-LOX were determined by semi-quan

175 Thus, BLT2, a unique receptor for 5-lipoxygenase- and cyclooxygenase-1-derived lipid media

176 eries of bone marrow chimeras generated from 5-lipoxygenase- and LTA(4) hydrolase-deficient mice, we

177 the utility of this approach by identifying 5-lipoxygenase as underlying previously identified quant

178 ic residues that 1) were common to different 5-lipoxygenases but not shared with other lipoxygenases,

179 tty acids including AA activated cPLA(2) and 5-lipoxygenase by increasing [Ca(2+)](i) and inducing cP

180 evated serum LTB4 and synovial expression of 5-lipoxygenase correlated with increased disease severit

181 Phosphorylation and redistribution of 5-lipoxygenase could be produced by overexpression of th

182 sfer of autoreactive T cells from B6 mice to 5-lipoxygenase-deficient (5-LO-/-) mice, which have a fu

183 5-Lipoxygenase-deficient (5-LOX(-/-)) mice, which displa

184 expression is partially reduced in infected 5-lipoxygenase-deficient [knockout (KO)] mice.

185 Retinas from diabetic 5-lipoxygenase-deficient mice also had significantly les

186 Wild-type mice, 5-lipoxygenase-deficient mice, and 12/15-lipoxygenase-de

187 al alterations were significantly reduced in 5-lipoxygenase-deficient mice, but not 12/15-lipoxygenas

188 istopathology was significantly inhibited in 5-lipoxygenase-deficient mice, but not in 12/15-lipoxyge

189 Recent findings indicate that 5-lipoxygenase-dependent (5-LO-dependent) lipoxins regul

190 fic NADP(+)-dependent dehydrogenase utilizes 5-lipoxygenase-derived 5-hydroxy-6,8,11,14-eicosatetraen

191 ellular lipid bodies of LTC(4), the dominant 5-lipoxygenase-derived eicosanoid in eosinophils.

192 redoxin reductase, and the overexpression of 5-lipoxygenase did not inhibit thioredoxin reductase or

193 n sequence, resulting in the accumulation of 5-lipoxygenase enzyme in the cytoplasm.

194 Human genetics have implicated the 5-lipoxygenase enzyme in the pathogenesis of cardiovascu

195 Ai knockdown or pharmacological block of the 5-lipoxygenase enzyme prevented activated mast cells fro

196 e infection model of GAS in mice lacking the 5-lipoxygenase enzyme to determine the role of endogenou

197 chidonic acid can then be metabolized by the 5-lipoxygenase enzyme to generate the proinflammatory si

198 ontained both leukotriene A(4) hydrolase and 5-lipoxygenase exclusively in the cytoplasm.

199 hVPLA2 also caused the translocation of 5-lipoxygenase from the cytosol to the nuclear membrane

200 also shifts the subcellular distribution of 5-lipoxygenase from the nucleus to the cytoplasm.

201 Both sites were found to be common to 5-lipoxygenases from different species but not found on

202 A promoter polymorphism in the 5-lipoxygenase gene affects gene expression and response

203 , we hypothesized that a polymorphism in the 5-lipoxygenase gene promoter could relate to atheroscler

204 Variant 5-lipoxygenase genotypes (lacking the common allele) wer

205 Variant 5-lipoxygenase genotypes identify a subpopulation with i

206 We determined 5-lipoxygenase genotypes, carotid-artery intima-media th

207 and its cytoplasmic targets HSP25/27, LSP-1, 5-lipoxygenase, glycogen synthase, and tyrosine hydroxyl

208 from arachidonic acid through the action of 5-lipoxygenase have been known for over two decades and

209 antagonists of the type 1 cysLT receptor or 5-lipoxygenase, implying that bronchoconstriction and MC

210 required to disable nuclear accumulation of 5-lipoxygenase in all cells.

211 leukotriene A(4) hydrolase co-localizes with 5-lipoxygenase in different types of leukocytes.

212 flux, and translocation of cPLA(2)alpha and 5-lipoxygenase in eosinophils.

213 e was also found to accumulate together with 5-lipoxygenase in the nucleus of alveolar macrophages.

214 Inhibition of the LTB4 biosynthetic enzyme 5-lipoxygenase inhibited toxin A-induced increases in il

215 s that were abrogated by anti-PlGF Ab or the 5-lipoxygenase inhibitor zileuton.

216 inhibitor; PIO+ATV and zileuton, a selective 5-lipoxygenase inhibitor; or zileuton alone.

217 5-Lipoxygenase inhibitors blocked IL-16-, eotaxin-, and

218 However, 5-lipoxygenase inhibitors, anti-IgE, and immunomodulator

219 and leukotriene C(4)) production, indicating 5-lipoxygenase inhibitory activities.

220 The enzyme 5-lipoxygenase initiates leukotriene synthesis; nuclear

221 The enzyme 5-lipoxygenase initiates the synthesis of leukotrienes f

222 5-Lipoxygenase is known to be present in the cytoplasm o

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

225 Phospholipase A2/5-lipoxygenase/leukotriene-B4 (PLA2/5-LOX/LTB4) axis is

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

228 ATP failed to decrease the parasitic load in 5-lipoxygenase (LO)-deficient macrophages.

229 We previously reported the infection of C3H 5-lipoxygenase (LO)-deficient mice with Borrelia burgdor

230 19-2, we co-expressed in human macrophages a 5-lipoxygenase (LOX) 3'UTR-luciferase reporter vector to

231 alization of the key SPM biosynthetic enzyme 5-lipoxygenase (LOX) in vascular cells.

232 trienes by targeting cyclooxygenases (COXs), 5-lipoxygenase (LOX), or the 5-LOX-activating protein (F

233 hese results indicate that nuclear import of 5-lipoxygenase may reflect the combined functional effec

234 Activation of NF-kappaB and 5-lipoxygenase-mediated (5-LO-mediated) biosynthesis of

235 , phosphorylated FTY720, or S1P also require 5-lipoxygenase-mediated synthesis of cysteinyl leukotrie

236 pe mice were enriched with receptors for the 5-lipoxygenase metabolite leukotriene B(4).

237 geted gene expression data demonstrated that 5-lipoxygenase metabolites correlated with the pathogeni

238 e results suggest that the concentrations of 5-lipoxygenase metabolites of arachidonic acid, 5-hydrox

239 y, also significant off-target reductions in 5-lipoxygenase metabolites.

240 The nuclear import of 5-lipoxygenase modulates its capacity to produce leukotr

241 tes leukotriene synthesis; nuclear import of 5-lipoxygenase modulates leukotriene synthetic capacity.

242 betic mice produced neither leukotrienes nor 5-lipoxygenase mRNA.

243 enase-activating protein rescues activity of 5-lipoxygenase mutations that delay nuclear membrane ass

244 led to have some effect on the inhibition of 5-lipoxygenase, no cytotoxicity against RAW 264.7 macrop

245 potent chemotactic agent synthesized by the 5-lipoxygenase of neutrophils.

246 way was ineffective, whereas blocking either 5-lipoxygenase of the lipoxygenase pathway or the cycloo

247 Protein kinase A phosphorylates 5-lipoxygenase on Ser(523), and this reduces its activit

248 lipoxygenase pathway either directly through 5'-lipoxygenase or via antagonism of the leukotriene B4

249 idonic acid converted to leukotrienes by the 5-lipoxygenase pathway activated in this cell.

250 tivating protein (FLAP) inhibitors attenuate 5-lipoxygenase pathway activity and reduce the productio

251 ns of proinflammatory lipid mediators of the 5-lipoxygenase pathway are significantly higher in MIAC

252 The 5-lipoxygenase pathway has been strongly implicated in t

253 TB4 biosynthesis following activation of the 5-lipoxygenase pathway in vivo.

254 The cysteinyl leukotrienes (cys-LTs) are 5-lipoxygenase pathway products implicated in asthma, in

255 Cysteinyl leukotrienes (cysLTs), 5-lipoxygenase pathway products, are recognized now not

256 east cancer cells produce metabolites of the 5-lipoxygenase pathway such as leukotriene B4 to activat

257 Here we show that by activating the 5-lipoxygenase pathway, M. tuberculosis not only inhibit

258 1 and 2 pathways and to leukotrienes via the 5-lipoxygenase pathway.

259 opose that PPARalpha in B cells and/or tumor 5-lipoxygenase pathways represents new targets for pharm

260 B(4) biosynthesis is to activate cPLA(2) and 5-lipoxygenase primarily by liberating from the outer pl

261 n of COX-2-derived prostanoids and augmented 5-lipoxygenase product formation, consistent with COX-2

262 11,14-eicosatetraenoic acid (5-oxo-ETE) is a 5-lipoxygenase product that acts via the selective OXE r

263 11,14-eicosatetraenoic acid (5-oxo-ETE) is a 5-lipoxygenase product that is a potent granulocyte chem

264 etic isoflurane attenuated the production of 5-lipoxygenase products and IL-10 and reduced CD11b and

265 derivatives reported here identify specific 5-lipoxygenase products as candidate physiologically rel

266 LTB4 was unique among 5-lipoxygenase products in this regard, since LTD4 and 5

267 verall capacity of whole blood to synthesize 5-lipoxygenase products; these genotype-related changes

268 IL-10, suggesting a direct link between the 5-lipoxygenase proinflammatory pathway and IL-10 regulat

269 -A4 and 15-epi-LXA4 levels and for COX-2 and 5-lipoxygenase protein expression.

270 sequence that can mediate nuclear import of 5-lipoxygenase remains to be identified.

271 5-Lipoxygenase represents a novel pathway for therapeuti

272 are generated by cyclooxygenase isozymes and 5-lipoxygenase, respectively, and their biosynthesis and

273 utative bipartite nuclear import sequence of 5-lipoxygenase revealed that this region formed an alpha

274 o and in a murine model of inflammation that 5-lipoxygenase stimulation induces PPAR-alpha signaling

275 arine n-3 fatty acids (including a competing 5-lipoxygenase substrate that reduces the production of

276 nteract with the dietary intake of competing 5-lipoxygenase substrates.

277 in attenuation of GAPDH downregulation, but 5-lipoxygenase suppression had no effect.

278 umans support a proinflammatory role for the 5-lipoxygenase system.

279 ry products of arachidonic acid oxidation by 5-lipoxygenase that have been shown to be involved in re

280 hin the nuclear localization sequence-518 of 5-lipoxygenase, the ability of protein kinase A to phosp

281 enes is tightly regulated, and expression of 5-lipoxygenase, the enzyme required for the first step i

282 marrow cells from nondiabetic mice expressed 5-lipoxygenase, the enzyme required for the initiation o

283 which we identify as a scaffold protein for 5-Lipoxygenase, the initial enzyme of LT synthesis.

284 o FLAP and subsequently being transferred to 5-lipoxygenase, thereby preventing leukotriene biosynthe

285 Unlike 5-lipoxygenase, these enzymes are expressed in most tiss

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

289 Human recombinant 5-lipoxygenase used both enantiomers as substrates, and

290 orylation was mediated by an upregulation of 5-lipoxygenase via cdk5 kinase pathway activation.

291 Finally, 5-lipoxygenase was discovered as an additional molecular

292 n corresponding to residues 518-530 on human 5-lipoxygenase was found to be unique to 5-lipoxygenase

293 Similarly, 5-lipoxygenase was localized in the nucleus of neutrophi

294 Myocardial expression of 5-lipoxygenase was not altered by PIO, ATV, or their com

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

297 In contrast, metabolites of 5-lipoxygenase were poor inhibitors of isolated thioredo

298 Animals lacking 5-lipoxygenase were significantly more vulnerable to int

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