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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
12                The cysteinyl leukotriene(1) (CysLT(1)) receptor antagonist montelukast significantly
13             In contrast to the dual CysLT(1)/CysLT(2) antagonist, BAY u9773, the CysLT(1) receptor-se
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
17 blish whether human T(H)2 cells are indeed a CysLT target cell type.
18 n, and pharmacological characterization of a CysLT receptor (CysLTR), which was identified by ligand
19                      The administration of a CysLT(1)R antagonist augmented the permeability response
20 r that has the expected characteristics of a CysLT(2) receptor.
21                                     Although CysLTs can induce the migration of fibrocytes in vitro,
22                                 CysLT(1) and CysLT(2) receptors colocalized to the plasma membranes a
23 n-coupled receptors, termed the CysLT(1) and CysLT(2) receptors.
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.
28  of CysLT receptors, designated CysLT(1) and CysLT(2).
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
32 MLP-mediated release of arachidonic acid and CysLT formation by eosinophils.
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
40 1 and type 2 cys-LT receptors (CysLT(1)R and CysLT(2)R, respectively).
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
43  CysLT(2)R negatively regulates LTC(4)S- and CysLT(1)R-dependent DC-mediated sensitization.
44 a displayed robust secretion of both EDN and CysLTs.
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
52 human skin fibroblasts, which was blocked by CysLT(2)R antagonism but not CysLT(1)R antagonism.
53 n in OVA-treated mice were also inhibited by CysLT(1) receptor blockade.
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
57 aracteristics of the thus far poorly defined CysLT(2) receptor.
58 ast two types of CysLT receptors, designated CysLT(1) and CysLT(2).
59                   The structurally different CysLT(1) receptor-selective antagonists zafirlukast, mon
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
62                      In contrast to the dual CysLT(1)/CysLT(2) antagonist, BAY u9773, the CysLT(1) re
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
66                                  We examined CysLT synthesis and arachidonic acid (AA) and lysophosph
67                         Although MCs express CysLT(2), their responses to cys-LTs are blocked by anta
68         Activation of endogenously expressed CysLT(1)R and CysLT(2)R occurred over an equimolar range
69 der of potency similar to that described for CysLT(1) (leukotriene [LT] D(4) > LTC(4) > LTE(4)).
70  a negative regulatory function of GPR17 for CysLT(1)R in a primary cell.
71 ems, revealing novel physiological roles for CysLT signaling.
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
74                                     Further, CysLTs directly potentiated IL-5 and IL-13 production fr
75 inflammatory responses in vivo, we generated CysLT(1)R-deficient mice by targeted gene disruption.
76                           Thus, we generated CysLT(2) receptor-deficient mice by targeted gene disrup
77 rough 2 G protein-coupled receptors (GPCRs), CysLT(1) and CysLT(2), which are coexpressed by most mye
78                           In particular, how CysLT(1)R expression and function are constitutively reg
79                                     However, CysLTs do appear to regulate the proliferation of fibroc
80                        The recombinant human CysLT(2) receptor was expressed in Xenopus oocytes and H
81                                    The human CysLT(1) receptor has been recently cloned and character
82  with 87.3% amino acid identity to the human CysLT(1) receptor.
83                                    The human CysLT(2) receptor gene is located on chromosome 13q14.12
84                  Recent data have implicated CysLTs in the establishment and amplification of T(H)2 r
85 asation was also significantly diminished in CysLT(1)R-deficient mice undergoing IgE-mediated passive
86                        A further increase in CysLT synthesis was induced by the addition of sPLA(2)-X
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
91      CysLT(2)R-deficient BMDCs had increased CysLT(1)R-dependent LTD(4)-induced ERK phosphorylation,
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
94 h N-methyl LTC(4) reduced D. farinae-induced CysLT(1)R expression on WT BMDCs.
95 bation with thyroid antigens did not inhibit CysLT production by mast cells.
96 d reduced responses in the genotypes lacking CysLT(1)R.
97 sponses were absent in MCs from mice lacking CysLT(1) receptors, but enhanced by the absence of CysLT
98 UVA) as determined by cysteinyl leukotriene (CysLT) production.
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
101 nd may participate in cysteinyl leukotriene (CysLT; C(4), D(4), and E(4)) synthesis.
102 + flux, secretion of cysteinyl leukotrienes (CysLT), and eosinophil-derived neurotoxin (EDN) release.
103                  The cysteinyl leukotrienes (CysLTs) are important mediators of human asthma.
104  vascular actions of cysteinyl leukotrienes (CysLTs) are mediated by 2 receptors: cysteinyl leukotrie
105                  The cysteinyl leukotrienes (CysLTs) are potent biological mediators in the pathophys
106                      Cysteinyl leukotrienes (CysLTs) are potent lipid mediators involved in bronchoco
107                      Cysteinyl leukotrienes (CysLTs) contribute to asthma pathogenesis, in part throu
108          Aerosolized cysteinyl leukotrienes (CysLTs) elicit migration of eosinophils into guinea pig
109                  The cysteinyl leukotrienes (CysLTs) have been implicated in the pathophysiology of i
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
112  eicosanoids such as cysteinyl leukotrienes (CysLTs).
113 induced secretion of cysteinyl leukotrienes (CysLTs).
114 agonist for the type 1 receptor for cys-LTs (CysLT(1)R), it was resistant to knockdown of this recept
115 ib is a novel anti-angiogenic small-molecule CysLT receptor antagonist.
116 tably expressing either isoform of the mouse CysLT(1) receptor cDNA.
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
119                       The gene for the mouse CysLT(1) receptor was mapped to band XD.
120 ar cloning and characterization of the mouse CysLT(2) receptor (mCysLT(2)R) from heart tissue.
121                            Endogenous murine CysLT(1) receptors also gave specific [(3)H]-ATLa bindin
122 centration-dependent manner, can inhibit non-CysLT(1)-mediated proinflammatory reactions, suggesting
123 induced Ca2+ fluxes and EDN release, but not CysLT secretion from circulating eosinophils.
124  was blocked by CysLT(2)R antagonism but not CysLT(1)R antagonism.
125 La proved to be a potent inhibitor (>50%) of CysLT(1)-mediated vascular leakage in murine skin (200 m
126 1) receptors, but enhanced by the absence of CysLT(2) receptors.
127 ation, whereas N-methyl LTC(4) activation of CysLT(2)R on WT BMDCs reduced such signaling.
128 vation and resulting in the amplification of CysLT synthesis during cPLA(2)alpha activation.
129 ses to cys-LTs are blocked by antagonists of CysLT(1).
130 ion for LTD(4) binding and as antagonists of CysLT(2) receptor signaling.
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
134 anation for the anti-inflammatory effects of CysLT(1) antagonists.
135 did not correlate with mucosal expression of CysLT(1) or CysLT(2).
136 LTC(4)S-dependent cell surface expression of CysLT(1)R on DCs.
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
139 the MAPK cascade leading to the formation of CysLT via cPLA2alpha.
140 so attenuated the fMLP-mediated formation of CysLT.
141 l-phenylalanine (fMLP)-mediated formation of CysLT.
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.
144                           We used a model of CysLT(1) signaling in human monocytes to characterize Cy
145 aused marked AA release and a rapid onset of CysLT synthesis in human eosinophils that was blocked by
146                       Negative regulation of CysLT(1)-induced mitogenic signaling responses of MCs 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
149 ested the existence of at least two types of CysLT receptors, designated CysLT(1) and CysLT(2).
150 bution of CysLT2R to the vascular actions of CysLTs has not been addressed.
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.
153 plays a significant role in the formation of CysLTs by human eosinophils.
154 ory environment may promote the formation of CysLTs through this mechanism.
155                     Endogenous production of CysLTs contributes to basal fibrocyte proliferation, but
156 onstitutive and aspirin-induced secretion of CysLTs that characterize this disorder.
157 synthesis that led to increased secretion of CysLTs.
158                                 Synthesis of CysLTs in response to sPLA(2)-X or lysophosphatidylcholi
159  cell surface CysLT(1)R was not increased on CysLT(2)R-deficient BMDCs, it was upregulated at 24 h by
160 elate with mucosal expression of CysLT(1) or CysLT(2).
161 y a pulse of D. farinae, compared with WT or CysLT(2)R/LTC(4)S-deficient BMDCs.
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
169 tophagoides farinae, via the type 1 receptor CysLT(1)R on dendritic cells (DCs).
170 , the role of the homologous type 2 receptor CysLT(2)R in Th2 immunity is unknown.
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
175 express both cysteinyl leukotriene receptor (CysLT) 1 and CysLT2.
176 iators acting on the type 1 cys-LT receptor (CysLT(1)R) to mediate smooth muscle constriction and vas
177 ficient mice but not type 1 cys-LT receptor (CysLT(1)R)-deficient mice.
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
182  defined type 1 and type 2 cys-LT receptors (CysLT(1)R and CysLT(2)R, respectively).
183 oth cysteinyl leukotriene (CysLT) receptors, CysLT(1) and CysLT(2,) were present in rat conjunctiva a
184                                  Recombinant CysLT(1) receptor gave stereospecific binding with both
185 diolabeled LTD(4) binding to the recombinant CysLT(2) receptor demonstrated high affinity binding and
186 ed through at least two distinct but related CysLT G protein-coupled receptors.
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
190 ays can be completely inhibited by selective CysLT(1) antagonists.
191  regulator for the CysLT(1)R that suppresses CysLT(1)R-mediated function at the cell membrane.
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
194                          We demonstrate that CysLT(2) interacts with CysLT(1), and that knockdown of
195 , or both CysLT(2)R/LTC(4)S, suggesting that CysLT(2)R negatively regulates LTC(4)S- and CysLT(1)R-de
196                                          The CysLT(1) receptor antagonist MK571 significantly decreas
197                                          The CysLT(1) receptor has been cloned recently.
198                                 Although the CysLT(1) receptor mediates the proinflammatory effects o
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
202                                  Because the CysLT(1) receptor blockers are effective in treating hum
203  response to LTE(4) in mice lacking both the CysLT(1)R and CysLT(2)R could establish the existence of
204  effect of LTD(4) was fully inhibited by the CysLT(1) receptor antagonist, MK-571.
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
214               The membrane expression of the CysLT(1)R analyzed by FACS with anti-Myc Ab was not redu
215        To clarify the different roles of the CysLT(1)R and CysLT(2)R in inflammatory responses in viv
216 t augmented the permeability response of the CysLT(1)R/CysLT(2)R double-deficient mice to LTC(4), LTD
217 in understanding the functional roles of the CysLT(2) receptor.
218 phil infiltration, cys-LT production, or the CysLT(2)R might be useful in the treatment of AD.
219 ne receptor, GPR17, negatively regulates the CysLT(1)R-mediated inflammatory cell accumulation in the
220 gent G protein-coupled receptors, termed the CysLT(1) and CysLT(2) receptors.
221 chronic injury might be mediated through the CysLT(2) receptor.
222  protein with 38% amino acid identity to the CysLT(1) receptor.
223 CysLT(1)/CysLT(2) antagonist, BAY u9773, the CysLT(1) receptor-selective antagonists MK-571, monteluk
224  cell mucous secretion with LTD(4) using the CysLT(1) receptor.
225 ooth muscle constrictors that signal via the CysLT(1) receptor.
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
228 blocked by pretreatment of the mice with the CysLT(1)R antagonist, MK-571.
229 activated receptors, here exemplified by the CysLTs, P2Y12, and P2Y14.
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
233                                        Thus, CysLT(2)R negatively regulates the development of cys-LT
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
236                          The clinically used CysLT(1) receptor antagonist, Singulair, showed a lower
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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