ライフサイエンスコーパス: CysLT

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 binds LTC(4) and LTD(4)in vitro with similar a

6 CysLT(2)R played a role in itch in the MC903 mouse model

7 CysLT(2)R-deficient BMDCs had increased CysLT(1)R-depend

8 CysLTs (LTD(4) and LTC(4)) induced an increased producti

9 CysLTs cooperate with IL-25 to activate ILC2s, and tuft-

10 CysLTs induced concentration dependent calcium mobilisat

11 CysLTs, particularly LTE4, are important contributors to

12 CysLTs, particularly LTE4, induced migration, reduced ap

13 -coupled receptors, cysteinyl leukotriene 1 (CysLT(1)) and CysLT(2) receptors, recently have been cha

14 d disruption of the cysteinyl leukotriene 1 (CysLT(1)) receptor suggested that the chronic injury mig

15 ity toward cysteinyl leukotriene receptor 1 (CysLT(1)R) and G-protein-coupled bile acid receptor 1 (G

16 The cysteinyl leukotriene(1) (CysLT(1)) receptor antagonist montelukast significantly

17 In contrast to the dual CysLT(1)/CysLT(2) antagonist, BAY u9773, the CysLT(1) receptor-se

18 og BAY u9773, reported to be a dual CysLT(1)/CysLT(2) antagonist, was found to be an antagonist at Cy

19 of cysteinyl leukotriene receptors 1 and 2 (CysLT(1) and CysLT(2)) and the PGE(2) receptors E-prosta

20 its signaling through the CysLT receptor 2 (CysLT(2)R) in itch.

21 Moreover, we have identified BAY u9773 as a CysLT(2) selective agonist, which could prove to be of i

22 blish whether human T(H)2 cells are indeed a CysLT target cell type.

23 n, and pharmacological characterization of a CysLT receptor (CysLTR), which was identified by ligand

24 The administration of a CysLT(1)R antagonist augmented the permeability response

25 r that has the expected characteristics of a CysLT(2) receptor.

26 ced pulmonary eosinophilia in mice through a CysLT(2)R-mediated, platelet- and IL-33-dependent pathwa

27 Although CysLTs can induce the migration of fibrocytes in vitro,

28 the IL-13-mediated upregulation of H(1) and CysLT(1) receptors, without showing an alteration of mus

29 CysLT(1) and CysLT(2) receptors colocalized to the plasma membranes a

30 n-coupled receptors, termed the CysLT(1) and CysLT(2) receptors.

31 biology and distribution of the CysLT(1) and CysLT(2) receptors; the functions of cys-LTs and their r

32 ene G protein-coupled receptors CysLT(1) and CysLT(2) regulate pro-inflammatory responses associated

33 her, basal expression levels of CysLT(1) and CysLT(2) were significantly higher in uninfected corneas

34 leukotriene receptors 1 and 2 (CysLT(1) and CysLT(2)) and the PGE(2) receptors E-prostanoid 1 to 4 (

35 cysteinyl leukotriene receptor, CysLT(1) and CysLT(2), have been identified and pharmacologically cha

36 s of two major CysLT receptors, CysLT(1) and CysLT(2), in the cornea using experimental mouse models

37 tein-coupled receptors (GPCRs), CysLT(1) and CysLT(2), which are coexpressed by most myeloid cells.

38 of CysLT receptors, designated CysLT(1) and CysLT(2).

39 leukotriene (CysLT) receptors, CysLT(1) and CysLT(2,) were present in rat conjunctiva and in rat and

40 tors, cysteinyl leukotriene 1 (CysLT(1)) and CysLT(2) receptors, recently have been characterized and

41 T(1)-transfected HEK293 cells and IL-10- and CysLT(1) small interfering RNA-induced downregulation of

42 MLP-mediated release of arachidonic acid and CysLT formation by eosinophils.

43 2) increases CysLT(1) surface expression and CysLT(1)-dependent proliferation of cord blood-derived h

44 orescence microscopy revealed that GPR17 and CysLT(1)R colocalize on the cell surface of human periph

45 s physiological receptor to induce itch, and CysLT(2)R contributes to itch in a model of dermatitis.

46 desensitization experiments in monocytes and CysLT(1)-transfected HEK293 cells and IL-10- and CysLT(1

47 TE(4) in mice lacking both the CysLT(1)R and CysLT(2)R could establish the existence of a separate LT

48 ear of mice deficient in both CysLT(1)R and CysLT(2)R elicits a vascular leak that exceeds the respo

49 ify the different roles of the CysLT(1)R and CysLT(2)R in inflammatory responses in vivo, we generate

50 tion of endogenously expressed CysLT(1)R and CysLT(2)R occurred over an equimolar range of LTD(4) and

51 1 and type 2 cys-LT receptors (CysLT(1)R and CysLT(2)R, respectively).

52 ittermates, which express both CysLT(1)R and CysLT(2)R, responded substantially to 1 x 10(-6) m LTD(4

53 he cysLTs, CysLT(1) receptor (CysLT(1)R) and CysLT(2)R, which are 38% homologous and are located on m

54 CysLT(2)R negatively regulates LTC(4)S- and CysLT(1)R-dependent DC-mediated sensitization.

55 ll mice (Cysltr2 (-/-)) compared with WT and CysLT(1)R-null mice (Cysltr1 (-/-)).

56 a displayed robust secretion of both EDN and CysLTs.

57 Inflammatory signaling induced by oLTs and CysLTs in human bronchial epithelial cells were compared

58 riction through the smooth muscle-associated CysLT type 1 receptor (CysLT1R), one of at least two loo

59 D(4) bind and compete with equal affinity at CysLT(1), providing a molecular basis for aspirin-trigge

60 antagonist, was found to be an antagonist at CysLT(1) sites but acted as a partial agonist at this ne

61 functionally antagonizes LTC(4) signaling at CysLT(2)R.

62 om wild-type littermates, which express both CysLT(1)R and CysLT(2)R, responded substantially to 1 x

63 TE(4) into the ear of mice deficient in both CysLT(1)R and CysLT(2)R elicits a vascular leak that exc

64 h2 pulmonary inflammation by inhibiting both CysLT(1)R signaling and D. farinae-induced LTC(4)S-depen

65 C(4) synthase (LTC(4)S), CysLT(1)R, or both CysLT(2)R/LTC(4)S, suggesting that CysLT(2)R negatively

66 human skin fibroblasts, which was blocked by CysLT(2)R antagonism but not CysLT(1)R antagonism.

67 n in OVA-treated mice were also inhibited by CysLT(1) receptor blockade.

68 uced mitogenic signaling responses of MCs by CysLT(2) demonstrates physiologically relevant functions

69 In WT recipients of LLC cells, CysLT(2)R expression is significantly increased in the t

70 signaling in human monocytes to characterize CysLT(1)-dependent and -independent anti-inflammatory ac

71 here are two mouse receptors for the cysLTs, CysLT(1) receptor (CysLT(1)R) and CysLT(2)R, which are 3

72 nd associated diseases for over two decades, CysLT(2)R has recently started to emerge as a potential

73 aracteristics of the thus far poorly defined CysLT(2) receptor.

74 ast two types of CysLT receptors, designated CysLT(1) and CysLT(2).

75 reactions occurs in 50% of reactions despite CysLT(1)R antagonist prophylaxis and identifies lung fun

76 The structurally different CysLT(1) receptor-selective antagonists zafirlukast, mon

77 te phenotypes and an influence on downstream CysLT receptor signaling pathways.

78 COX-1 was dispensable for FcepsilonRI-driven CysLT production.

79 the inflammatory milieu that in part drives CysLT overproduction and, in particular, the role of IFN

80 iene analog BAY u9773, reported to be a dual CysLT(1)/CysLT(2) antagonist, was found to be an antagon

81 In contrast to the dual CysLT(1)/CysLT(2) antagonist, BAY u9773, the CysLT(1) re

82 ures of CysLT(2)R in complex with three dual CysLT(1)R/CysLT(2)R antagonists.

83 Further, inhibition of either CysLT receptor converted the disease response of both st

84 response to exogenous LTC4 and to endogenous CysLTs evoked by passive cutaneous anaphylaxis was augme

85 polymerase chain reaction, markedly enhanced CysLT-stimulated intracellular calcium mobilization comp

86 netic and pharmacological findings establish CysLT(2)R as a gateway for angiogenesis and EC dysregula

87 f mCysLT(2)R will be useful for establishing CysLT(2)R-deficient mice and determining novel leukotrie

88 We examined CysLT synthesis and arachidonic acid (AA) and lysophosph

89 Although MCs express CysLT(2), their responses to cys-LTs are blocked by anta

90 Activation of endogenously expressed CysLT(1)R and CysLT(2)R occurred over an equimolar range

91 der of potency similar to that described for CysLT(1) (leukotriene [LT] D(4) > LTC(4) > LTE(4)).

92 a negative regulatory function of GPR17 for CysLT(1)R in a primary cell.

93 stration of LTE(4), the preferred ligand for CysLT(3)R, was additive with LTC(4).

94 ems, revealing novel physiological roles for CysLT signaling.

95 ings suggest a novel mechanism of action for CysLTs in the pathogenesis of asthma and provide a poten

96 0(-6) m LTC(4), whereas the macrophages from CysLT(1)R-deficient mice did not respond to either LTD(4

97 Further, CysLTs directly potentiated IL-5 and IL-13 production fr

98 inflammatory responses in vivo, we generated CysLT(1)R-deficient mice by targeted gene disruption.

99 Thus, we generated CysLT(2) receptor-deficient mice by targeted gene disrup

100 rough 2 G protein-coupled receptors (GPCRs), CysLT(1) and CysLT(2), which are coexpressed by most mye

101 age, and metastases in WT mice, highlighting CysLT(2)R as a VEGF-independent regulator of the vascula

102 In particular, how CysLT(1)R expression and function are constitutively reg

103 However, CysLTs do appear to regulate the proliferation of fibroc

104 The recombinant human CysLT(2) receptor was expressed in Xenopus oocytes and H

105 The human CysLT(1) receptor has been recently cloned and character

106 with 87.3% amino acid identity to the human CysLT(1) receptor.

107 The human CysLT(2) receptor gene is located on chromosome 13q14.12

108 Recent data have implicated CysLTs in the establishment and amplification of T(H)2 r

109 asation was also significantly diminished in CysLT(1)R-deficient mice undergoing IgE-mediated passive

110 A further increase in CysLT synthesis was induced by the addition of sPLA(2)-X

111 l infiltration, was significantly reduced in CysLT(1)R-deficient mice subjected to zymosan A-induced

112 ollagen fibers, was significantly reduced in CysLT(2) receptor-null mice as compared with the wild-ty

113 ous anaphylaxis was significantly reduced in CysLT(2) receptor-null mice as compared with wild-type m

114 oma (LLC) cells are significantly reduced in CysLT(2)R-null mice (Cysltr2 (-/-)) compared with WT and

115 A and lysophospholipid release, resulting in CysLT synthesis in eosinophils through a mechanism invol

116 for synthesis of all eicosanoids, including CysLTs.

117 CysLT(2)R-deficient BMDCs had increased CysLT(1)R-dependent LTD(4)-induced ERK phosphorylation,

118 1), and that knockdown of CysLT(2) increases CysLT(1) surface expression and CysLT(1)-dependent proli

119 ells responded selectively to the individual CysLTs, LTC(4), LTD(4), or LTE(4), with a calcium mobili

120 h N-methyl LTC(4) reduced D. farinae-induced CysLT(1)R expression on WT BMDCs.

121 bation with thyroid antigens did not inhibit CysLT production by mast cells.

122 d reduced responses in the genotypes lacking CysLT(1)R.

123 sponses were absent in MCs from mice lacking CysLT(1) receptors, but enhanced by the absence of CysLT

124 of histamine H(1) and cysteinyl leukotriene CysLT(1) receptors.

125 UVA) as determined by cysteinyl leukotriene (CysLT) production.

126 We found that both cysteinyl leukotriene (CysLT) receptors, CysLT(1) and CysLT(2,) were present in

127 administration of the cysteinyl leukotriene (CysLT)1 receptor antagonist montelukast, the corticoster

128 nd may participate in cysteinyl leukotriene (CysLT; C(4), D(4), and E(4)) synthesis.

129 + flux, secretion of cysteinyl leukotrienes (CysLT), and eosinophil-derived neurotoxin (EDN) release.

130 Here we show that cysteinyl-leukotrienes (CysLT) released by HIV-infected or HIVgp120 stimulated M

131 The cysteinyl leukotrienes (CysLTs) are important mediators of human asthma.

132 Cysteinyl leukotrienes (CysLTs) are lipid mediators that drive type 2 inflammati

133 vascular actions of cysteinyl leukotrienes (CysLTs) are mediated by 2 receptors: cysteinyl leukotrie

134 The cysteinyl leukotrienes (CysLTs) are potent biological mediators in the pathophys

135 Cysteinyl leukotrienes (CysLTs) are potent lipid mediators involved in bronchoco

136 Cysteinyl leukotrienes (CysLTs) are potent prophlogistic mediators in asthmatic

137 Cysteinyl leukotrienes (CysLTs) contribute to asthma pathogenesis, in part throu

138 Aerosolized cysteinyl leukotrienes (CysLTs) elicit migration of eosinophils into guinea pig

139 Cysteinyl leukotrienes (CysLTs) have been defined as central mediators of inflam

140 The cysteinyl leukotrienes (CysLTs) have been implicated in the pathophysiology of i

141 Cysteinyl leukotrienes (CysLTs), comprising LTC(4), LTD(4), and LTE(4), are prod

142 n of proinflammatory cysteinyl leukotrienes (CysLTs), defective generation of anti-inflammatory prost

143 atory actions of the cysteinyl leukotrienes (CysLTs), LTC(4), LTD(4), and LTE(4), are thought to be m

144 d mediators, such as cysteinyl leukotrienes (CysLTs), which are present in asthma, could further ampl

145 eicosanoids such as cysteinyl leukotrienes (CysLTs).

146 induced secretion of cysteinyl leukotrienes (CysLTs).

147 agonist for the type 1 receptor for cys-LTs (CysLT(1)R), it was resistant to knockdown of this recept

148 xamined the expression profiles of two major CysLT receptors, CysLT(1) and CysLT(2), in the cornea us

149 In MC903-treated mice, CysLT levels increased in skin over time, and Cysltr2(-/

150 ib is a novel anti-angiogenic small-molecule CysLT receptor antagonist.

151 tably expressing either isoform of the mouse CysLT(1) receptor cDNA.

152 model human diseases, we isolated the mouse CysLT(1) receptor from a mouse lung cDNA library and fou

153 rthern blot analysis revealed that the mouse CysLT(1) receptor mRNA is expressed in lung and skin; an

154 The gene for the mouse CysLT(1) receptor was mapped to band XD.

155 ar cloning and characterization of the mouse CysLT(2) receptor (mCysLT(2)R) from heart tissue.

156 Endogenous murine CysLT(1) receptors also gave specific [(3)H]-ATLa bindin

157 centration-dependent manner, can inhibit non-CysLT(1)-mediated proinflammatory reactions, suggesting

158 induced Ca2+ fluxes and EDN release, but not CysLT secretion from circulating eosinophils.

159 was blocked by CysLT(2)R antagonism but not CysLT(1)R antagonism.

160 La proved to be a potent inhibitor (>50%) of CysLT(1)-mediated vascular leakage in murine skin (200 m

161 1) receptors, but enhanced by the absence of CysLT(2) receptors.

162 ation, whereas N-methyl LTC(4) activation of CysLT(2)R on WT BMDCs reduced such signaling.

163 vation and resulting in the amplification of CysLT synthesis during cPLA(2)alpha activation.

164 ses to cys-LTs are blocked by antagonists of CysLT(1).

165 ion for LTD(4) binding and as antagonists of CysLT(2) receptor signaling.

166 and may underlie the therapeutic benefit of CysLT receptor antagonists, such as pranlukast, in this

167 D. farinae sensitization and challenge of CysLT(2)R-deficient mice showed a marked augmentation of

168 ll interfering RNA-induced downregulation of CysLT(1) expression, we showed that reported CysLT(1) ag

169 anation for the anti-inflammatory effects of CysLT(1) antagonists.

170 did not correlate with mucosal expression of CysLT(1) or CysLT(2).

171 LTC(4)S-dependent cell surface expression of CysLT(1)R on DCs.

172 s) increased both the membrane expression of CysLT(1)R protein by FACS analysis and the LTD(4)-elicit

173 ation studies indicate highest expression of CysLT(2) receptors in adrenal glands, heart, and placent

174 the MAPK cascade leading to the formation of CysLT via cPLA2alpha.

175 so attenuated the fMLP-mediated formation of CysLT.

176 l-phenylalanine (fMLP)-mediated formation of CysLT.

177 n asthmatic patients; however, inhibition of CysLT receptor 1 is not a consistently effective treatme

178 While selective inhibition of CysLT(1)R has been used for treating asthma and associat

179 teracts with CysLT(1), and that knockdown of CysLT(2) increases CysLT(1) surface expression and CysLT

180 Postinfection, disparate levels of CysLT receptors were accompanied by distinct expression

181 Further, basal expression levels of CysLT(1) and CysLT(2) were significantly higher in uninf

182 the agonist-mediated calcium mobilization of CysLT(2) receptors at physiological concentrations.

183 We used a model of CysLT(1) signaling in human monocytes to characterize Cy

184 We used 2 different in vivo models of CysLT(2)R-dependent immunopathology, as well as ex vivo

185 aused marked AA release and a rapid onset of CysLT synthesis in human eosinophils that was blocked by

186 Negative regulation of CysLT(1)-induced mitogenic signaling responses of MCs by

187 reveal a constitutive negative regulation of CysLT(1)R functions by GPR17 in both the Ag presentation

188 in human asthma, the physiological roles of CysLT(2) receptor are not defined, and a suitable mouse

189 Here, we describe four crystal structures of CysLT(2)R in complex with three dual CysLT(1)R/CysLT(2)R

190 of these findings, therapeutic targeting of CysLT receptors extends beyond inhibition of proinflamma

191 ested the existence of at least two types of CysLT receptors, designated CysLT(1) and CysLT(2).

192 bution of CysLT2R to the vascular actions of CysLTs has not been addressed.

193 ely activated by nanomolar concentrations of CysLTs with a rank order potency of LTC(4) = LTD(4) >> L

194 ed detection of distinct vascular effects of CysLTs, which can be mediated via the CysLT2R in vivo.

195 plays a significant role in the formation of CysLTs by human eosinophils.

196 ory environment may promote the formation of CysLTs through this mechanism.

197 Endogenous production of CysLTs contributes to basal fibrocyte proliferation, but

198 onstitutive and aspirin-induced secretion of CysLTs that characterize this disorder.

199 synthesis that led to increased secretion of CysLTs.

200 Synthesis of CysLTs in response to sPLA(2)-X or lysophosphatidylcholi

201 These effects did not depend on CysLT(1)R.

202 cell surface CysLT(1)R was not increased on CysLT(2)R-deficient BMDCs, it was upregulated at 24 h by

203 elate with mucosal expression of CysLT(1) or CysLT(2).

204 y a pulse of D. farinae, compared with WT or CysLT(2)R/LTC(4)S-deficient BMDCs.

205 show that airway challenges with the parent CysLT, leukotriene C4 (LTC4), given in combination with

206 ddition, fibrocytes are capable of producing CysLTs and can be regulated via the autocrine or paracri

207 ed cysteinyl leukotriene receptor 1 protein (CysLT(1)) expression using calcium flux, cyclic AMP, and

208 ed by adoptive transfer of D. farinae-pulsed CysLT(2)R-deficient bone marrow-derived DCs (BMDCs) also

209 , which has characteristics of the purported CysLT(1) receptor subtype, should assist in the elucidat

210 sLT(2)R in complex with three dual CysLT(1)R/CysLT(2)R antagonists.

211 imately 64-fold more potent in the CysLT(1)R/CysLT(2)R double-deficient mice than in sufficient mice.

212 d the permeability response of the CysLT(1)R/CysLT(2)R double-deficient mice to LTC(4), LTD(4), and L

213 tophagoides farinae, via the type 1 receptor CysLT(1)R on dendritic cells (DCs).

214 , the role of the homologous type 2 receptor CysLT(2)R in Th2 immunity is unknown.

215 to noncysteinyl leukotriene type 1 receptor (CysLT(1))-mediated inhibitory mechanisms that have been

216 receptors for the cysLTs, CysLT(1) receptor (CysLT(1)R) and CysLT(2)R, which are 38% homologous and a

217 encing and demonstrate that LTD(4) receptor (CysLT(1)) is induced in human vascular endothelia by int

218 endogenous adipocyte G(q)-coupled receptor (CysLT(2) receptor) greatly improved glucose and lipid ho

219 or platelet-specific type 2 cysLT receptor (CysLT(2)R) completely eliminated both platelet activatio

220 f the type 1 cysteinyl leukotriene receptor (CysLT(1)R) are efficacious for bronchoconstriction in hu

221 express both cysteinyl leukotriene receptor (CysLT) 1 and CysLT2.

222 iators acting on the type 1 cys-LT receptor (CysLT(1)R) to mediate smooth muscle constriction and vas

223 ficient mice but not type 1 cys-LT receptor (CysLT(1)R)-deficient mice.

224 TC(4)S-deficient and type 2 cys-LT receptor (CysLT(2)R)-deficient mice but not type 1 cys-LT receptor

225 o classes of cysteinyl leukotriene receptor, CysLT(1) and CysLT(2), have been identified and pharmaco

226 f the second cysteinyl leukotriene receptor, CysLT(2), a 346-amino acid protein with 38% amino acid i

227 establish the existence of a third receptor, CysLT(E)R, that responds preferentially to LTE(4), the m

228 inyl leukotriene G protein-coupled receptors CysLT(1) and CysLT(2) regulate pro-inflammatory response

229 defined type 1 and type 2 cys-LT receptors (CysLT(1)R and CysLT(2)R, respectively).

230 ssion profiles of two major CysLT receptors, CysLT(1) and CysLT(2), in the cornea using experimental

231 oth cysteinyl leukotriene (CysLT) receptors, CysLT(1) and CysLT(2,) were present in rat conjunctiva a

232 Recombinant CysLT(1) receptor gave stereospecific binding with both

233 diolabeled LTD(4) binding to the recombinant CysLT(2) receptor demonstrated high affinity binding and

234 ed through at least two distinct but related CysLT G protein-coupled receptors.

235 CysLT(1) expression, we showed that reported CysLT(1) agonists leukotriene D(4) and UDP signal throug

236 GPR17 with Myc-tagged CysLT(1)R, the robust CysLT(1)R-mediated calcium response to LTD(4) was abolis

237 lacking leukotriene C(4) synthase (LTC(4)S), CysLT(1)R, or both CysLT(2)R/LTC(4)S, suggesting that Cy

238 atelets were all were blocked by a selective CysLT(2)R antagonist and inhibited by LTD(4).

239 Administration of a selective CysLT(2)R antagonist significantly reduced LLC tumor vol

240 ays can be completely inhibited by selective CysLT(1) antagonists.

241 Our data suggest CysLT(2)R as a possible target for intervention.

242 regulator for the CysLT(1)R that suppresses CysLT(1)R-mediated function at the cell membrane.

243 ough the baseline expression of cell surface CysLT(1)R was not increased on CysLT(2)R-deficient BMDCs

244 ctions of 6xHis-tagged GPR17 with Myc-tagged CysLT(1)R, the robust CysLT(1)R-mediated calcium respons

245 We demonstrate that CysLT(2) interacts with CysLT(1), and that knockdown of

246 We found that CysLT(2)R regulates angiogenesis in isolated mouse endot

247 ular hyperpermeability, we hypothesized that CysLT(2)R, via its actions on the endothelium, might reg

248 , or both CysLT(2)R/LTC(4)S, suggesting that CysLT(2)R negatively regulates LTC(4)S- and CysLT(1)R-de

249 The CysLT(1) receptor antagonist MK571 significantly decreas

250 The CysLT(1) receptor has been cloned recently.

251 Although the CysLT(1) receptor mediates the proinflammatory effects o

252 reased for exosomes from asthmatics, and the CysLT(1) receptor antagonist Montelukast reduced exosome

253 hetic enzymes, transporter proteins, and the CysLT(1) receptor, diverse functions of cys-LTs and thei

254 role for eosinophil-derived cys-LTs and the CysLT(2)R in the hyperkeratosis and fibrosis of allergic

255 Because the CysLT(1) receptor blockers are effective in treating hum

256 response to LTE(4) in mice lacking both the CysLT(1)R and CysLT(2)R could establish the existence of

257 effect of LTD(4) was fully inhibited by the CysLT(1) receptor antagonist, MK-571.

258 onse to a particular pathobiologic event the CysLT(2) receptor can mediate an increase in vascular pe

259 mobilization in HEK-293 cells expressing the CysLT receptor was not affected by pertussis toxin, and

260 mobilization in HEK-293 cells expressing the CysLT receptor were potently inhibited by the structural

261 eptor, and by uncovering a dual role for the CysLT(1) receptor, namely proinflammatory acute constric

262 ent, constitutive negative regulator for the CysLT(1)R that suppresses CysLT(1)R-mediated function at

263 is approximately 64-fold more potent in the CysLT(1)R/CysLT(2)R double-deficient mice than in suffic

264 fter bleomycin injection were similar in the CysLT(2) receptor-null mice and the wild-type mice.

265 Components of the CysLT pathway are differentially regulated in brains of

266 he molecular biology and distribution of the CysLT(1) and CysLT(2) receptors; the functions of cys-LT

267 In contrast, targeted disruption of the CysLT(1) receptor significantly increased both the conce

268 The membrane expression of the CysLT(1)R analyzed by FACS with anti-Myc Ab was not redu

269 To clarify the different roles of the CysLT(1)R and CysLT(2)R in inflammatory responses in viv

270 t augmented the permeability response of the CysLT(1)R/CysLT(2)R double-deficient mice to LTC(4), LTD

271 in understanding the functional roles of the CysLT(2) receptor.

272 phil infiltration, cys-LT production, or the CysLT(2)R might be useful in the treatment of AD.

273 ne receptor, GPR17, negatively regulates the CysLT(1)R-mediated inflammatory cell accumulation in the

274 gent G protein-coupled receptors, termed the CysLT(1) and CysLT(2) receptors.

275 ole for LTC(4) and its signaling through the CysLT receptor 2 (CysLT(2)R) in itch.

276 chronic injury might be mediated through the CysLT(2) receptor.

277 protein with 38% amino acid identity to the CysLT(1) receptor.

278 CysLT(1)/CysLT(2) antagonist, BAY u9773, the CysLT(1) receptor-selective antagonists MK-571, monteluk

279 cell mucous secretion with LTD(4) using the CysLT(1) receptor.

280 ooth muscle constrictors that signal via the CysLT(1) receptor.

281 c inflammation with fibrosis, likely via the CysLT(2) receptor, and by uncovering a dual role for the

282 sorders, in particular asthma, for which the CysLT receptor antagonists pranlukast, zafirlukast, and

283 blocked by pretreatment of the mice with the CysLT(1)R antagonist, MK-571.

284 activated receptors, here exemplified by the CysLTs, P2Y12, and P2Y14.

285 ation of the pathophysiological roles of the CysLTs and in the identification of additional receptor

286 macologic and clinical studies show that the CysLTs exert most of their bronchoconstrictive and proin

287 , our study reveals that LTC(4) acts through CysLT(2)R as its physiological receptor to induce itch,

288 CysLT receptor-mediated inflammation through CysLT-like inflammatory biological activities previously

289 signaling in T(H)2 cells is mediated through CysLT(1) coupled to G(alpha)q and G(alpha)i proteins, an

290 of potentially deleterious signaling through CysLT(2)R, and it may contribute to the therapeutic prop

291 Thus, CysLT(2)R negatively regulates the development of cys-LT

292 Presumably oLTs contribute to CysLT receptor-mediated inflammation through CysLT-like

293 )-X may be an important mechanism leading to CysLT formation in the airways of patients with asthma.

294 lished proinflammatory activities related to CysLT receptor activation, results generated from BALB/c

295 an T(H)2 cells are selectively responsive to CysLTs in a calcium flux assay when compared with T(H)1

296 l activities previously ascribed uniquely to CysLTs.

297 The clinically used CysLT(1) receptor antagonist, Singulair, showed a lower

298 monocytes/macrophages or mast cells utilize CysLT(1)R for the response of the microvasculature in ac

299 s serving as a local damper of both vascular CysLT(1) signals as well as ALX receptor-regulated polym

300 s in healthy human lungs were MCTRs, whereas CysLTs were most prevalent in patients with disease.

301 ased in the tumor vasculature, compared with CysLT(1)R.

302 We demonstrate that CysLT(2) interacts with CysLT(1), and that knockdown of CysLT(2) increases CysLT