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1 ically active dose of fMLP (5 x 10(-9) M) or leukotriene B(4) (1 x 10(-7) M) in the presence of a phy
2 d miR-219-5p expression along with increased leukotriene B(4) (5-fold) and decreased (~3-fold) specia
3 (FR), platelet-activating factor (PAFR), and leukotriene B(4) (BLTR) were transfected into RBL-2H3 ce
4 whether 15-epi-LXA(4) (anti-inflammatory) or leukotriene B(4) (inflammatory mediator) is produced.
5 ic steps: increased arachidonic acid-derived leukotriene B(4) (LTB(4)) and decreased 5S-hydroxyeicosa
6 te requirement for the lipid chemoattractant leukotriene B(4) (LTB(4)) and its receptor BLT1 for neut
8 ecific binding to human PMN was displaced by leukotriene B(4) (LTB(4)) and LTB(4) receptor 1 (BLT1) a
9 V phospholipase A(2) (hVPLA(2)) could elicit leukotriene B(4) (LTB(4)) biosynthesis in human neutroph
19 a lead optimization effort starting with the leukotriene B(4) (LTB(4)) receptor antagonist (2), membe
20 ple chemoattractant receptors, including the leukotriene B(4) (LTB(4)) receptor BLT1 and the chemokin
22 Current immunoassays for the measurement of leukotriene B(4) (LTB(4)) typically utilize an enzyme-li
23 ation of leukotriene synthesis, and produced leukotriene B(4) (LTB(4)) when stimulated with the calci
24 ls, vitamin E forms differentially inhibited leukotriene B(4) (LTB(4)) with an IC(50) of 5-20 muM for
25 catalyzes the final step in the synthesis of leukotriene B(4) (LTB(4)), a potent chemoattractant and
27 (cys-LTs), prostaglandin E(2) (PGE(2)), and leukotriene B(4) (LTB(4)), and also 8-isoprostane as a m
29 hil influx, along with cytokines/chemokines, leukotriene B(4) (LTB(4)), and vascular cell adhesion mo
31 r, the role of CXCL1 in mediating neutrophil leukotriene B(4) (LTB(4)), reactive oxygen species (ROS)
32 LTA(4)H knockdown limited the formation of leukotriene B(4) (LTB(4)), the enzymatic product of LTA(
39 acrophage migration inhibitory factor (MIF), leukotriene B(4) (LTB4), and high mobility group box 1 p
40 activity (p < 0.002) and the chemoattractant leukotriene B(4) (p < 0.02), which fell from a median ba
41 5-oxoprostaglandin 13-reductase, also termed leukotriene B(4) 12-hydroxydehydrogenase (PGR/LTB(4)DH),
44 , GST Mu 5, a hypothetical GST Mu, GST Pi B, leukotriene B(4) 12-hydroxydehydrogenase, and proteasome
45 ammatory reactions investigated (elicited by leukotriene B(4) [LTB(4)], CXCL1, tumor necrosis factor
47 zymosan-stimulated PMN showed predominantly leukotriene B(4) and 20-OH-leukotriene B(4), as well as
48 tic increase (>50-fold) in the production of leukotriene B(4) and 5-hydroxyeicosatetraenoic acid, sig
51 bited calcium ionophore-induced leukotriene (leukotriene B(4) and leukotriene C(4)) production, indic
54 rgoing apoptosis produced similar amounts of leukotriene B(4) and significantly greater amounts of PG
55 but not Epac-1, suppressed AM production of leukotriene B(4) and TNF-alpha, whereas stimulation of e
57 nd protein excretion) and ex vivo glomerular leukotriene B(4) biosynthesis at 3 hr, and up to 4 days,
58 0 4F3 (CYP4F3) catalyzes the inactivation of leukotriene B(4) by omega-oxidation in human neutrophils
59 date cells showed no detectable responses to leukotriene B(4) confirming the deletion of the BLT1/BLT
60 ine phosphorylation of Vav1, whereas IL-8 or leukotriene B(4) did not, correlating with the requireme
63 ith significant reductions in the release of leukotriene B(4) from stimulated neutrophils and of inte
70 ls with the chemotactic peptide fMLP or with leukotriene B(4) or fibrinogen results in little increas
72 olic phospholipase A(2) (cPLA(2)) to produce leukotriene B(4) or with cyclooxygenase-2 (COX2) to prod
73 eutrophil fatty acid composition and ex vivo leukotriene B(4) production from stimulated neutrophils
74 its high-affinity G protein-coupled receptor leukotriene B(4) receptor 1 (BLT1) direct dectin-1-depen
75 is study, we report that the LTB(4) receptor leukotriene B(4) receptor 1 (BLT1) redistributes from no
77 ated an important role for the high-affinity leukotriene B(4) receptor BLT1 in arthritis, atheroscler
79 onstrated marked expression of 5-LOX and the leukotriene B(4) receptor in human pancreatic cancer tis
80 (+) monocytes in wild-type mice that express leukotriene B(4) receptor, BLT-1, and that this increase
82 ors with opposing functions, namely ALXR and leukotriene B(4) receptors (BLTs), revealed that the sev
84 crease by approximately 300% in 4 h, whereas leukotriene B(4) stimulated PMN to migrate the full thic
90 ammatory derivatives (prostaglandin E(2) and leukotriene B(4)) and an increased anti-inflammatory der
92 ment in vivo in response to eotaxin, but not leukotriene B(4), a phenomenon that could be prevented b
93 icosatetraenoic acids and, most importantly, leukotriene B(4), an inflammatory mediator involved in l
95 the synovial fluid, TNF-alpha, IL-8, PGE(2), leukotriene B(4), and leukotriene C(4) levels were signi
96 taxis to formylmethionylleucylphenylalanine, leukotriene B(4), and platelet-activating factor was com
97 PG)E(2) and 5-lipoxygenase-derived products, leukotriene B(4), and the biosynthesis interaction produ
98 wed predominantly leukotriene B(4) and 20-OH-leukotriene B(4), as well as lipoxin marker 5,15-diHETE.
99 nt by C5a in vivo required amplification via leukotriene B(4), because both C5a-mediated leukocyte re
100 resences of four different chemoattractants (leukotriene B(4), chemokine C-X-C motif ligands 2 and 8,
101 hod allows prostaglandins, thromboxane B(2), leukotriene B(4), hydroxyeicosatetraenoic acid isomers,
102 entrations and was associated with a fall in leukotriene B(4), which is thought to be central to the
103 age activation in vivo and the production of leukotriene B(4), which was required for optimal immune
104 tes (PMN) in vitro chemotaxis in response to leukotriene B(4), with the maximum inhibition ( approxim
105 n of lesional FLAP in myeloid cells promotes leukotriene B(4)-dependent VSMC phenotypic modulation, i
106 ally stable LXA(4) analog potently inhibited leukotriene B(4)-induced superoxide anion generation, th
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