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1 actor that acts on plasma membrane cysteinyl leukotriene receptors.
2 Our data show that LTB4, via its receptor B leukotriene receptor 1 (BLT1) and Galphai signaling, inc
4 ease in cell-surface expression of cysteinyl leukotriene receptor 1 (CysLT1) as determined by flow cy
5 rthermore, LTD4 plus PGE2, through cysteinyl leukotriene receptor 1 (CysLT1R) and E-prostanoid recept
7 " neutrophil subset that expressed cysteinyl leukotriene receptor 1 (CysLTR1) and produced TNF, CCL2,
11 tory cells and their expression of cysteinyl leukotriene receptors 1 and 2 (CysLT(1) and CysLT(2)) an
13 get VEGF receptors but antagonizes cysteinyl leukotriene receptors 1 and 2 (CysLT1-2) at micromolar I
15 d a recurrent mutation in CYSLTR2 (cysteinyl leukotriene receptor 2) encoding a p.Leu129Gln substitut
17 stain cytoplasmic Ca(2+) signaling following leukotriene receptor activation both by refilling the Ca
18 fter rundown of the Ca(2+) signals following leukotriene receptor activation, stimulation of P2Y rece
19 ukast (an antagonist of the type 1 cysteinyl leukotriene receptor) also inhibited E. coli invasion of
20 e as a dualistic uracil nucleotide/cysteinyl leukotriene receptor and by others as inactive toward th
21 ccelerated homologous desensitization of the leukotriene receptor and thereby terminated the oscillat
22 -lipoxygenase inhibition and sulfidopeptidyl leukotriene receptor antagonism on lumenal chemotaxis of
23 steroid (ICS step-up therapy) or addition of leukotriene receptor antagonist (LTRA step-up therapy) o
24 ment with ICSs alone (n = 1758) or ICSs plus leukotriene receptor antagonist (LTRAs; n = 354) or ICSs
25 ge in FEV1 in the Characterizing Response to Leukotriene Receptor Antagonist and Inhaled Corticostero
26 ium Respimat added to ICSs with or without a leukotriene receptor antagonist in a phase III trial in
27 yclo-oxygenase inhibitor indomethacin or the leukotriene receptor antagonist MK-571, indicating that
28 o examine a potential protective role of the leukotriene receptor antagonist montelukast on future ri
29 ected animals with MC-stabilizing drugs or a leukotriene receptor antagonist restores vascular integr
31 nist, long-acting muscarinic antagonist, and leukotriene receptor antagonist was hospitalized with a
32 choconstriction by a single oral dose of the leukotriene receptor antagonist zafirlukast was assessed
33 We aimed to assess whether montelukast, a leukotriene receptor antagonist, can improve symptoms or
34 vide benefit if combined with montelukast, a leukotriene receptor antagonist, in patients whose sympt
35 he effectiveness of montelukast, a cysteinyl leukotriene receptor antagonist, in the treatment of pos
36 for a daily inhaled corticosteroid, a daily leukotriene receptor antagonist, or a mast cell stabiliz
41 to ICS background therapy, with or without a leukotriene receptor antagonist; long-acting beta2-agoni
42 fluticasone twice daily plus 5 or 10 mg of a leukotriene-receptor antagonist daily (LTRA step-up).
43 We evaluated the ability of montelukast, a leukotriene-receptor antagonist, to protect such patient
44 roids (21.5%; 95% CI: 20.7%-22.3%; p<0.001), leukotriene receptor antagonists (13.4%; 95% CI: 12.9%-1
49 hieved by LABAs (improved lung function) and leukotriene receptor antagonists (LTRAs; protection agai
51 osteroids [topical (swallowed) or systemic], leukotriene receptor antagonists and, most recently, bio
54 agents such as cromolyn and the new class of leukotriene receptor antagonists have demonstrated benef
55 ukotriene synthesis inhibitors and cysteinyl leukotriene receptor antagonists have shown efficacy in
56 nical efficacy of inhaled glucocorticoids to leukotriene receptor antagonists in children with mild t
58 daily inhaled corticosteroids (ICSs), daily leukotriene receptor antagonists, and as-needed ICS trea
59 include daily inhaled corticosteroids, daily leukotriene receptor antagonists, and combination therap
60 s, long-acting inhaled beta2-stimulants, and leukotriene receptor antagonists, increased year after y
64 useful add-on therapies for AR include oral leukotriene receptor antagonists, short bursts of a nasa
65 emists in the design of potent and selective leukotriene receptor antagonists-leukotriene structural
69 ay disease include the use of muscarinic and leukotriene receptor antagonists; however, these pharmac
76 long-acting beta agonists, theophyllines, or leukotriene-receptor antagonists, adjusted stepwise acco
80 and characterization of the second cysteinyl leukotriene receptor, CysLT(2), a 346-amino acid protein
81 enes C4 associated with an overexpression of leukotrienes receptor CysLTR1 by asthmatic BSM cells in
82 kotriene B4 (LTB4R and LTB4R2) and cysteinyl leukotriene receptors (CYSLTR1 and CYSLTR2) contribute t
85 s of diabetes for retinal histopathology and leukotriene receptor expression and 2) after 3 months of
87 s the way for future clinical translation of leukotriene receptor inhibition for the treatment of dem
88 blotting for gene and protein expression of leukotriene receptors LT1-R and LT2-R, and for concentra
89 dministration has issued safety alerts about leukotriene receptor-modifying agents and suicidality/su
90 ing to replenish the PIP2 pool accessible to leukotriene receptors, ostensibly through control of PIP
91 a marketed anti-asthmatic drug antagonizing leukotriene receptors, reduces neuroinflammation, elevat
92 therosclerosis is associated with a specific leukotriene receptor(s) capable of inducing hyperreactiv
93 This work illustrates that inhibition of leukotriene receptor signalling might represent a safe a
97 ajor findings were: 1) protein levels of all leukotriene receptors were significantly increased in es
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