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1 rts leukotriene C4 (LTC4) to leukotriene D4 (LTD4).
2 e MBD-3 cleaves cystinyl-bis-glycine but not LTD4.
3 ring segments were unresponsive to LTC4 and LTD4.
4 al coronary arteries in response to LTC4 and LTD4.
5 mes greater than that of the natural ligand, LTD4.
6 fect signaling by methacholine, thrombin, or LTD4.
12 s, leukotriene C4 (LTC4) and leukotriene D4 (LTD4) also provoked PMN-endothelial cell adhesion, but v
13 -lipoxygenase products in this regard, since LTD4 and 5-hydroxyeicosatetraenoic acid (HETE) were unab
14 lar leak to intradermal injection of LTC4 or LTD4 and an augmented response to LTE4 as compared with
15 ized the effects of exogenously administered LTD4 and cysLTs released endogenously in response to phy
16 triene (cysLT) LTC4, which is converted into LTD4 and finally to LTE4 after extracellular transport.
17 n (calcium mobilization) of this receptor by LTD4 and LTC4, and competition for radiolabelled LTD4 bi
19 eicosatetraenoic acid, and its metabolites, LTD4 and LTE4, are lipid mediators of smooth muscle cons
22 were observed in AERD (at 60 min for PGD2 , LTD4 , and LTE4 ) but not in MNSAID-UA or control subjec
26 trienes-leukotriene C4(LTC4), leukotriene D4(LTD4) and leukotriene E4(LTE4)-are important mediators o
27 of leukotriene C4 (LTC4) and leukotriene D4 (LTD4) and their binding activity in both atherosclerotic
28 eukotrienes (cysLTs), leukotriene C4 (LTC4), LTD4, and LTE4 are proinflammatory lipid mediators with
30 of peptidoleukotrienes (leukotriene [LT] C4, LTD4, and LTE4) was measured in esophageal circular musc
31 leukotrienes (cys-LTs; leukotriene [LT] C4, LTD4, and LTE4), and prostaglandin (PG) E2 are generated
32 ising the cysteinyl leukotrienes (LTs; LTC4, LTD4, and LTE4), only LTE4 is stable and abundant in viv
33 nes (cysLTs), including leukotriene (LT) C4, LTD4, and LTE4, are metabolites of arachidonic acid and
34 ed PI production and calcium mobilization by LTD4, and significantly attenuated the effects of PKC in
36 inhibitor nordihydro-guaiaretic acid and the LTD4 antagonist ICI 198,615 inhibited ACh-induced contra
37 the drug-glutathione S-conjugate DNP-SG, the LTD4 antagonist MK571 and arsenate were also competitive
38 l-glutathione, oxidized glutathione, and the LTD4 antagonist MK571 were competitive inhibitors of dau
39 conjugate APA-SG, oxidized glutathione, the LTD4 antagonist MK571, arsenate, and genistein were comp
42 and LTC4, and competition for radiolabelled LTD4 binding to this receptor by the cysteinyl leukotrie
47 TD4 raises the possibility that clearance of LTD4 during asthma and in related inflammatory condition
51 e exposed to aerosols of 0.3 to 30 microg/ml LTD4 for 1 min, during which specific airway conductance
53 pe 1 cys-LT receptor (CysLT1R), and LTC4 and LTD4 have similar lesser potency for CysLT2R, whereas LT
56 istologic characteristics of leukotriene D4 (LTD4)-induced eosinophil influx into the airways of cons
60 mma (1,000 U/ml for 24 h) markedly increased LTD4-induced changes in cell stiffness, from 4.6 +/- 1 [
61 neally), produced dose-related inhibition of LTD4-induced eosinophilia, measured in 24 h or 3 wk BAL,
64 swell chamber experiments and also augmented LTD4-induced production of monocyte chemotactic protein
67 not differ between the groups, but levels of LTD4 , LTE4 , and PGD2 were significantly higher in AERD
69 eviously reported proinflammatory effects of LTD4 may contribute significantly to its overall influen
71 ed rats, this concentration of intracellular LTD4 neither raised intracellular Ca2+ nor activated the
73 we determined the effect of leukotriene D4 (LTD4) on the function of Na,K-ATPase in alveolar epithel
74 s article, we demonstrate that LTC4, but not LTD4 or LTE4, activates mouse platelets exclusively thro
82 with granulocytes before it is converted to LTD4, promoting mediator generation and the formation of
83 ation of a second enzyme capable of cleaving LTD4 raises the possibility that clearance of LTD4 durin
85 uaiaretic acid, the specific leukotriene D4 (LTD4) receptor antagonist MK-571, and the 5-lipoxygenase
88 these data suggest that IFN-gamma increases LTD4 responses in HASM cells by increasing cell-surface
89 ed vascular permeability, but not to LTC4 or LTD4, revealing a preference of GPR99 for LTE4 even when
90 d with both [3H]LXA4 and [3H]leukotriene D4 (LTD4)-specific binding in vitro to neutrophils and endot
91 or human monocytes, PKC inhibition augmented LTD4-stimulated calcium flux and cell migration assessed
92 ion of endogenous CysLT1Rs augments multiple LTD4-stimulated cellular functions, with associated incr
93 ontraction ex vivo, PKC inhibition augmented LTD4-stimulated contraction, and increased phosphoinosit
95 ervations demonstrate that the conversion of LTD4 to LTE4 and the degradation of cys-bis-gly are cata
96 utant mice retain partial ability to convert LTD4 to LTE4, ranging from 80-90% of the wild-type value
98 ression in HASM, cell stiffness responses to LTD4 were measured with magnetic twisting cytometry.
99 ction and calcium mobilization stimulated by LTD4 yet had almost no effect on H1 histamine receptor i
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