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1 CysLT synthesis mediated by sPLA(2)-X but not AA release
2 CysLT(1) and CysLT(2) receptors colocalized to the plasm
3 CysLT(1)R and GPR17 expressed in transfected cells were
4 CysLT(2) receptor mRNA was detected in lung macrophages
5 CysLT(2)R-deficient BMDCs had increased CysLT(1)R-depend
6 CysLTs (LTD(4) and LTC(4)) induced an increased producti
7 CysLTs induced concentration dependent calcium mobilisat
8 CysLTs, particularly LTE4, are important contributors to
9 CysLTs, particularly LTE4, induced migration, reduced ap
10 -coupled receptors, cysteinyl leukotriene 1 (CysLT(1)) and CysLT(2) receptors, recently have been cha
11 d disruption of the cysteinyl leukotriene 1 (CysLT(1)) receptor suggested that the chronic injury mig
14 og BAY u9773, reported to be a dual CysLT(1)/CysLT(2) antagonist, was found to be an antagonist at Cy
15 of cysteinyl leukotriene receptors 1 and 2 (CysLT(1) and CysLT(2)) and the PGE(2) receptors E-prosta
16 Moreover, we have identified BAY u9773 as a CysLT(2) selective agonist, which could prove to be of i
18 n, and pharmacological characterization of a CysLT receptor (CysLTR), which was identified by ligand
24 biology and distribution of the CysLT(1) and CysLT(2) receptors; the functions of cys-LTs and their r
25 leukotriene receptors 1 and 2 (CysLT(1) and CysLT(2)) and the PGE(2) receptors E-prostanoid 1 to 4 (
26 cysteinyl leukotriene receptor, CysLT(1) and CysLT(2), have been identified and pharmacologically cha
27 tein-coupled receptors (GPCRs), CysLT(1) and CysLT(2), which are coexpressed by most myeloid cells.
29 leukotriene (CysLT) receptors, CysLT(1) and CysLT(2,) were present in rat conjunctiva and in rat and
30 tors, cysteinyl leukotriene 1 (CysLT(1)) and CysLT(2) receptors, recently have been characterized and
31 T(1)-transfected HEK293 cells and IL-10- and CysLT(1) small interfering RNA-induced downregulation of
33 2) increases CysLT(1) surface expression and CysLT(1)-dependent proliferation of cord blood-derived h
34 orescence microscopy revealed that GPR17 and CysLT(1)R colocalize on the cell surface of human periph
35 desensitization experiments in monocytes and CysLT(1)-transfected HEK293 cells and IL-10- and CysLT(1
36 TE(4) in mice lacking both the CysLT(1)R and CysLT(2)R could establish the existence of a separate LT
37 ear of mice deficient in both CysLT(1)R and CysLT(2)R elicits a vascular leak that exceeds the respo
38 ify the different roles of the CysLT(1)R and CysLT(2)R in inflammatory responses in vivo, we generate
39 tion of endogenously expressed CysLT(1)R and CysLT(2)R occurred over an equimolar range of LTD(4) and
41 ittermates, which express both CysLT(1)R and CysLT(2)R, responded substantially to 1 x 10(-6) m LTD(4
42 he cysLTs, CysLT(1) receptor (CysLT(1)R) and CysLT(2)R, which are 38% homologous and are located on m
45 riction through the smooth muscle-associated CysLT type 1 receptor (CysLT1R), one of at least two loo
46 D(4) bind and compete with equal affinity at CysLT(1), providing a molecular basis for aspirin-trigge
47 antagonist, was found to be an antagonist at CysLT(1) sites but acted as a partial agonist at this ne
48 om wild-type littermates, which express both CysLT(1)R and CysLT(2)R, responded substantially to 1 x
49 TE(4) into the ear of mice deficient in both CysLT(1)R and CysLT(2)R elicits a vascular leak that exc
50 h2 pulmonary inflammation by inhibiting both CysLT(1)R signaling and D. farinae-induced LTC(4)S-depen
51 C(4) synthase (LTC(4)S), CysLT(1)R, or both CysLT(2)R/LTC(4)S, suggesting that CysLT(2)R negatively
54 uced mitogenic signaling responses of MCs by CysLT(2) demonstrates physiologically relevant functions
55 signaling in human monocytes to characterize CysLT(1)-dependent and -independent anti-inflammatory ac
56 here are two mouse receptors for the cysLTs, CysLT(1) receptor (CysLT(1)R) and CysLT(2)R, which are 3
60 the inflammatory milieu that in part drives CysLT overproduction and, in particular, the role of IFN
61 iene analog BAY u9773, reported to be a dual CysLT(1)/CysLT(2) antagonist, was found to be an antagon
63 response to exogenous LTC4 and to endogenous CysLTs evoked by passive cutaneous anaphylaxis was augme
64 polymerase chain reaction, markedly enhanced CysLT-stimulated intracellular calcium mobilization comp
65 f mCysLT(2)R will be useful for establishing CysLT(2)R-deficient mice and determining novel leukotrie
72 ings suggest a novel mechanism of action for CysLTs in the pathogenesis of asthma and provide a poten
73 0(-6) m LTC(4), whereas the macrophages from CysLT(1)R-deficient mice did not respond to either LTD(4
75 inflammatory responses in vivo, we generated CysLT(1)R-deficient mice by targeted gene disruption.
77 rough 2 G protein-coupled receptors (GPCRs), CysLT(1) and CysLT(2), which are coexpressed by most mye
85 asation was also significantly diminished in CysLT(1)R-deficient mice undergoing IgE-mediated passive
87 l infiltration, was significantly reduced in CysLT(1)R-deficient mice subjected to zymosan A-induced
88 ollagen fibers, was significantly reduced in CysLT(2) receptor-null mice as compared with the wild-ty
89 ous anaphylaxis was significantly reduced in CysLT(2) receptor-null mice as compared with wild-type m
90 A and lysophospholipid release, resulting in CysLT synthesis in eosinophils through a mechanism invol
92 1), and that knockdown of CysLT(2) increases CysLT(1) surface expression and CysLT(1)-dependent proli
93 ells responded selectively to the individual CysLTs, LTC(4), LTD(4), or LTE(4), with a calcium mobili
97 sponses were absent in MCs from mice lacking CysLT(1) receptors, but enhanced by the absence of CysLT
99 We found that both cysteinyl leukotriene (CysLT) receptors, CysLT(1) and CysLT(2,) were present in
100 administration of the cysteinyl leukotriene (CysLT)1 receptor antagonist montelukast, the corticoster
102 + flux, secretion of cysteinyl leukotrienes (CysLT), and eosinophil-derived neurotoxin (EDN) release.
104 vascular actions of cysteinyl leukotrienes (CysLTs) are mediated by 2 receptors: cysteinyl leukotrie
110 atory actions of the cysteinyl leukotrienes (CysLTs), LTC(4), LTD(4), and LTE(4), are thought to be m
111 d mediators, such as cysteinyl leukotrienes (CysLTs), which are present in asthma, could further ampl
114 agonist for the type 1 receptor for cys-LTs (CysLT(1)R), it was resistant to knockdown of this recept
117 model human diseases, we isolated the mouse CysLT(1) receptor from a mouse lung cDNA library and fou
118 rthern blot analysis revealed that the mouse CysLT(1) receptor mRNA is expressed in lung and skin; an
122 centration-dependent manner, can inhibit non-CysLT(1)-mediated proinflammatory reactions, suggesting
125 La proved to be a potent inhibitor (>50%) of CysLT(1)-mediated vascular leakage in murine skin (200 m
131 and may underlie the therapeutic benefit of CysLT receptor antagonists, such as pranlukast, in this
132 D. farinae sensitization and challenge of CysLT(2)R-deficient mice showed a marked augmentation of
133 ll interfering RNA-induced downregulation of CysLT(1) expression, we showed that reported CysLT(1) ag
137 s) increased both the membrane expression of CysLT(1)R protein by FACS analysis and the LTD(4)-elicit
138 ation studies indicate highest expression of CysLT(2) receptors in adrenal glands, heart, and placent
142 teracts with CysLT(1), and that knockdown of CysLT(2) increases CysLT(1) surface expression and CysLT
143 the agonist-mediated calcium mobilization of CysLT(2) receptors at physiological concentrations.
145 aused marked AA release and a rapid onset of CysLT synthesis in human eosinophils that was blocked by
147 reveal a constitutive negative regulation of CysLT(1)R functions by GPR17 in both the Ag presentation
148 in human asthma, the physiological roles of CysLT(2) receptor are not defined, and a suitable mouse
151 ely activated by nanomolar concentrations of CysLTs with a rank order potency of LTC(4) = LTD(4) >> L
152 ed detection of distinct vascular effects of CysLTs, which can be mediated via the CysLT2R in vivo.
159 cell surface CysLT(1)R was not increased on CysLT(2)R-deficient BMDCs, it was upregulated at 24 h by
162 show that airway challenges with the parent CysLT, leukotriene C4 (LTC4), given in combination with
163 ddition, fibrocytes are capable of producing CysLTs and can be regulated via the autocrine or paracri
164 ed cysteinyl leukotriene receptor 1 protein (CysLT(1)) expression using calcium flux, cyclic AMP, and
165 ed by adoptive transfer of D. farinae-pulsed CysLT(2)R-deficient bone marrow-derived DCs (BMDCs) also
166 , which has characteristics of the purported CysLT(1) receptor subtype, should assist in the elucidat
167 imately 64-fold more potent in the CysLT(1)R/CysLT(2)R double-deficient mice than in sufficient mice.
168 d the permeability response of the CysLT(1)R/CysLT(2)R double-deficient mice to LTC(4), LTD(4), and L
171 to noncysteinyl leukotriene type 1 receptor (CysLT(1))-mediated inhibitory mechanisms that have been
172 receptors for the cysLTs, CysLT(1) receptor (CysLT(1)R) and CysLT(2)R, which are 38% homologous and a
173 encing and demonstrate that LTD(4) receptor (CysLT(1)) is induced in human vascular endothelia by int
174 f the type 1 cysteinyl leukotriene receptor (CysLT(1)R) are efficacious for bronchoconstriction in hu
176 iators acting on the type 1 cys-LT receptor (CysLT(1)R) to mediate smooth muscle constriction and vas
178 TC(4)S-deficient and type 2 cys-LT receptor (CysLT(2)R)-deficient mice but not type 1 cys-LT receptor
179 o classes of cysteinyl leukotriene receptor, CysLT(1) and CysLT(2), have been identified and pharmaco
180 f the second cysteinyl leukotriene receptor, CysLT(2), a 346-amino acid protein with 38% amino acid i
181 establish the existence of a third receptor, CysLT(E)R, that responds preferentially to LTE(4), the m
183 oth cysteinyl leukotriene (CysLT) receptors, CysLT(1) and CysLT(2,) were present in rat conjunctiva a
185 diolabeled LTD(4) binding to the recombinant CysLT(2) receptor demonstrated high affinity binding and
187 CysLT(1) expression, we showed that reported CysLT(1) agonists leukotriene D(4) and UDP signal throug
188 GPR17 with Myc-tagged CysLT(1)R, the robust CysLT(1)R-mediated calcium response to LTD(4) was abolis
189 lacking leukotriene C(4) synthase (LTC(4)S), CysLT(1)R, or both CysLT(2)R/LTC(4)S, suggesting that Cy
192 ough the baseline expression of cell surface CysLT(1)R was not increased on CysLT(2)R-deficient BMDCs
193 ctions of 6xHis-tagged GPR17 with Myc-tagged CysLT(1)R, the robust CysLT(1)R-mediated calcium respons
195 , or both CysLT(2)R/LTC(4)S, suggesting that CysLT(2)R negatively regulates LTC(4)S- and CysLT(1)R-de
199 reased for exosomes from asthmatics, and the CysLT(1) receptor antagonist Montelukast reduced exosome
200 hetic enzymes, transporter proteins, and the CysLT(1) receptor, diverse functions of cys-LTs and thei
201 role for eosinophil-derived cys-LTs and the CysLT(2)R in the hyperkeratosis and fibrosis of allergic
203 response to LTE(4) in mice lacking both the CysLT(1)R and CysLT(2)R could establish the existence of
205 onse to a particular pathobiologic event the CysLT(2) receptor can mediate an increase in vascular pe
206 mobilization in HEK-293 cells expressing the CysLT receptor was not affected by pertussis toxin, and
207 mobilization in HEK-293 cells expressing the CysLT receptor were potently inhibited by the structural
208 eptor, and by uncovering a dual role for the CysLT(1) receptor, namely proinflammatory acute constric
209 ent, constitutive negative regulator for the CysLT(1)R that suppresses CysLT(1)R-mediated function at
210 is approximately 64-fold more potent in the CysLT(1)R/CysLT(2)R double-deficient mice than in suffic
211 fter bleomycin injection were similar in the CysLT(2) receptor-null mice and the wild-type mice.
212 he molecular biology and distribution of the CysLT(1) and CysLT(2) receptors; the functions of cys-LT
213 In contrast, targeted disruption of the CysLT(1) receptor significantly increased both the conce
216 t augmented the permeability response of the CysLT(1)R/CysLT(2)R double-deficient mice to LTC(4), LTD
219 ne receptor, GPR17, negatively regulates the CysLT(1)R-mediated inflammatory cell accumulation in the
223 CysLT(1)/CysLT(2) antagonist, BAY u9773, the CysLT(1) receptor-selective antagonists MK-571, monteluk
226 c inflammation with fibrosis, likely via the CysLT(2) receptor, and by uncovering a dual role for the
227 sorders, in particular asthma, for which the CysLT receptor antagonists pranlukast, zafirlukast, and
230 ation of the pathophysiological roles of the CysLTs and in the identification of additional receptor
231 macologic and clinical studies show that the CysLTs exert most of their bronchoconstrictive and proin
232 signaling in T(H)2 cells is mediated through CysLT(1) coupled to G(alpha)q and G(alpha)i proteins, an
234 )-X may be an important mechanism leading to CysLT formation in the airways of patients with asthma.
235 an T(H)2 cells are selectively responsive to CysLTs in a calcium flux assay when compared with T(H)1
237 monocytes/macrophages or mast cells utilize CysLT(1)R for the response of the microvasculature in ac
238 s serving as a local damper of both vascular CysLT(1) signals as well as ALX receptor-regulated polym
239 We demonstrate that CysLT(2) interacts with CysLT(1), and that knockdown of CysLT(2) increases CysLT
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