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1 for ECP, tryptase, PGE2 , PGD2 , LTD4 , and LTE4 .
2 ed concentrations of urinary leukotriene E4 (LTE4).
3 of leukotriene D4 (LTD4) to leukotriene E4 (LTE4).
4 ia and the highest concentrations of urinary LTE4.
5 complexes with another receptor to recognize LTE4.
6 vel receptor that preferentially responds to LTE4.
9 e, we demonstrate that LTC4, but not LTD4 or LTE4, activates mouse platelets exclusively through CysL
13 tory actions of the stable abundant mediator LTE4 and is a novel potential therapeutic target for ast
14 EpC function and suggest that inhibition of LTE4 and of GPR99 may have therapeutic benefits in asthm
15 s demonstrate that the conversion of LTD4 to LTE4 and the degradation of cys-bis-gly are catalyzed by
16 fer between the groups, but levels of LTD4 , LTE4 , and PGD2 were significantly higher in AERD group.
17 nes (cys-LTs; leukotriene [LT] C4, LTD4, and LTE4), and prostaglandin (PG) E2 are generated at the si
18 to comprehensively define the roles of PGD2, LTE4, and their combination in activating human TH2 cell
20 In animal models, these drugs inhibit LTD4-, LTE4-, and antigen-induced bronchoconstriction, reduce i
21 s (cysLTs), leukotriene C4 (LTC4), LTD4, and LTE4 are proinflammatory lipid mediators with pathobiolo
23 C4), leukotriene D4(LTD4) and leukotriene E4(LTE4)-are important mediators of human bronchial asthma.
25 traenoic acid, and its metabolites, LTD4 and LTE4, are lipid mediators of smooth muscle constriction
26 s), including leukotriene (LT) C4, LTD4, and LTE4, are metabolites of arachidonic acid and mediate in
29 intracellular calcium signalling induced by LTE4 but did not restore full agonist responses at the g
30 ition between radiolabeled ADP and unlabeled LTE4 but not for direct binding of LTE4, suggesting that
31 ved in AERD (at 60 min for PGD2 , LTD4 , and LTE4 ) but not in MNSAID-UA or control subjects (P < 0.0
38 ling elicited by Alternaria or by intranasal LTE4 GPR99 expression is detected on lung and nasal EpCs
45 CysLT1 as a receptor responsible for potent LTE4-induced response in LAD2 but not in LUVA cells, an
48 ant alleles had significantly higher urinary LTE4 levels (38 vs. 30 nmol/mol creatinine, P = 0.0134),
49 ased cysLT exposure as determined by urinary LTE4 levels, reduced lung function and potentially worse
52 he purinergic receptor P2Y12 is required for LTE4 mediated pulmonary inflammation in a mouse model of
54 ed kinase (Erk) activation, are required for LTE4-mediated regulation of gene expression in human cel
55 99(-/-) mice showed a dose-dependent loss of LTE4-mediated vascular permeability, but not to LTC4 or
57 nasal EpCs, which release mucin to doses of LTE4 one log lower than that required to elicit submucos
60 otriene (LT)E4 , induced sputum fluid LTB4 , LTE4 , PGD2 , and PGE2 , plasma secretory phospholipase
62 ce retain partial ability to convert LTD4 to LTE4, ranging from 80-90% of the wild-type values in sma
67 unlabeled LTE4 but not for direct binding of LTE4, suggesting that P2Y12 complexes with another recep
76 leukotrienes (leukotriene [LT] C4, LTD4, and LTE4) was measured in esophageal circular muscle tissue.
77 Significant increases in PGD2 , LTD4 , and LTE4 were observed in AERD (at 60 min for PGD2 , LTD4 ,
78 re selected that differentially responded to LTE4 when analysed by intracellular signalling and gene
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