ライフサイエンスコーパス: A(3) receptor

1 a modulator of cell growth (mainly acting at A3 receptors).

2 e is not coupled to the xanthine-insensitive A3 receptor.

3 e cardioprotective role of a novel adenosine A3 receptor.

4 ture MDDCs as native expressers of the human A3 receptor.

5 AB-MECA binding confirmed the site to be the A3 receptor.

6 and which had a Ki value of 248 nM at human A3 receptors.

7 yl analogue was clearly less potent at human A3 receptors.

8 to enhance potency and selectivity at human A3 receptors.

9 gues were nearly equipotent at rat and human A3 receptors.

10 1 and A2A receptors and at recombinant human A3 receptors.

11 measurable affinity at adenosine A1, A2A, or A3 receptors.

12 ne) has high affinity for recombinant A1 and A3 receptors.

13 ting the presence of phospholipase C-coupled A3 receptors.

14 e, genistein, also bound only very weakly at A3 receptors.

15 receptors, respectively, and 3.0 nM at human A3 receptors.

16 m intracellular stores via the activation of A3 receptors.

17 thesized and found to be selective for human A3 receptors.

18 ed to arginine, the homologous amino acid in A3 receptors.

19 dioligands to recombinant canine A1, A2A, or A3 receptors.

20 t A1 and A2A receptors and 3 microM at human A3 receptors.

21 wed 14-fold greater affinity at human vs rat A3 receptors.

22 r affinity but 15-fold selectivity for human A3 receptors.

23 tors, respectively, and 3.25 microM at human A3 receptors.

24 increased selectivity of flavonols for human A3 receptors.

25 (Ki = 14 nM), while it lacks affinity at rat A3 receptors.

26 , had Ki values of 0.3 - 0.4 microM at human A3 receptors.

27 5-ethyl diester was > 600-fold selective for A3 receptors.

28 l cyclase in CHO cells expressing cloned rat A3 receptors.

29 its complete selectivity toward A1, A2A, and A3 receptors.

30 the anti-ischemic effect of adenosine A1 and A3 receptors.

31 chieve the anti-ischemic effect of adenosine A3 receptors.

32 Neither cells expressed A1 or A3 receptors.

33 selective enhancement of agonist binding at A3 receptors.

34 effect that is mediated by adenosine A1 and A3 receptors.

35 transfected with a vector encoding the human A(3) receptor.

36 transfected with the human adenosine A(1) or A(3) receptor.

37 evels of selectivity for the human adenosine A(3) receptor.

38 ffect in the heart via activation of A(1) or A(3) receptors.

39 otent than the (4S,2'R)-isomer in binding to A(3) receptors.

40 ions failed to improve potency in binding at A(3) receptors.

41 d a progressive reduction in the affinity at A(3) receptors.

42 ically to modify ligand affinity at A(1) and A(3) receptors.

43 losteric modulator of the adenosine A(1) and A(3) receptors.

44 tors, with no involvement of A(1), A(2B), or A(3) receptors.

45 protein for A(2A) and A(2B), but not A(1) or A(3) receptors.

46 ced lung mast cell degranulation by engaging A(3) receptors.

47 er to the 3-position lowered the affinity at A3 receptors 3-fold.

48 The adenosine-A(3) receptor (A(3)AR) is a G protein-coupled receptor t

49 The A(3) receptor (A(3)R) was found to be expressed in eosin

50 e contribution of A(1) receptors (A(1)R) and A(3) receptors (A(3)R) is not known.

51 cological or genetic inactivation of the ADO A(3) receptor, A(3)R, prevents CXCL16 effect.

52 ctivity and stability of the human adenosine A3 receptor (A3) were investigated.

53 previous work, using a fluorescent adenosine-A3 receptor (A3AR) agonist and fluorescence correlation

54 Adenosine A3 receptor (A3AR) having an identical N-terminal region

55 tion and degranulation of mast cells via the A3 receptor (A3AR).

56 Thus, adenosine A2B and A3 receptors act in a functional cooperative fashion to

57 ized adenosine in mice occur largely through A(3) receptor activation and that mast cells contribute

58 eptors was employed as a functional index of A3 receptor activation.

59 The A3 receptor (ADORA3) was expressed only in mouse islets

60 etalloproteinase (MMP)2, MMP7, and adenosine A3 receptor (ADORA3).

61 oropropyl ester (26) was favorable for human A3 receptor affinity, resulting in Ki values of 4.2 and

62 s in vivo was tested by exposing mice to the A(3) receptor agonist, IB-MECA.

63 nophils with the highly potent and selective A3 receptor agonist CI-IB-MECA clearly induced Ca2+ rele

64 BK-induced responses were unaffected by the A3 receptor agonist IB-MECA (1 microM).

65 2-chloro-N6-cyclopentyladenosine (CCPA) and A3 receptor agonist N6-(3-iodobenzyl)-adenosine-5'-N-met

66 In addition, the A3 receptor agonist N6-(3-iodobenzyl)adenosine-5'-N-meth

67 ophil membranes were characterized using the A3 receptor agonist radioligand 125I-labeled AB-MECA, wh

68 terized the actions of a selective adenosine A3 receptor agonist, 2-chloro-N6-(3-lodobenzyl)-adenosin

69 lopentyladenosine and not with the selective A3-receptor agonist 4-aminobenzyl-5'-N methylcarboxamido

70 d reduced affinity for most of the uncharged A(3) receptor agonists and antagonists examined.

71 general approach for the design of A(1) and A(3) receptor agonists having favorable pharmacodynamic

72 Selective A(1) and A(3) receptor agonists were shown to activate phospholip

73 new binary conjugates of adenosine A(1) and A(3) receptor agonists were synthesized and tested in a

74 t of the concentration-response curve of the A3 receptor agonists in the presence of antagonist and,

75 ist 2-Chloro-N6-cyclopentyladenosine and the A3 receptor agonists N6-Benzyl-NECA and 1-deoxy-1-[6-[[(

76 gineered atrial cells, in which either human A(3) receptors alone or both human A(1) and A(3) recepto

77 olin-5-yl]benzene acetamide (MRS1220) at the A(3) receptor and xanthine amine congener (XAC) and XAC-

78 Activation and blockade of adenosine A(2b)/A(3) receptors and activation and inhibition of protein

79 ly selective for the A(2A) over the A(1) and A(3) receptors and were more potent than MRE-0470 and CG

80 ryonic kidney 293 cells expressing the human A3 receptor and a chimeric Galphaq-i3 protein, which was

81 it is natural to consider a link between the A3 receptor and eosinophils.

82 ocytes with enhanced expression of the human A3 receptor and showed significantly higher ATP content,

83 tive, 28, displayed a Ki value of 31.4 nM at A3 receptors and 1300-fold selectivity vs A1 receptors.

84 Cardiac atrial cells lack native A3 receptors and exhibit a shorter duration of cardiopro

85 nd the compound is thus nonselective between A3 receptors and L-type Ca2+ channels.

86 44, displayed a Ki value of 7.94 nM at human A3 receptors and selectivity of 5200-fold.

87 poxia, ischemia, or seizures), activation of A3 receptors and subsequent heterologous desensitization

88 displayed a Ki value of 4.8 microM at human A3 receptors and was inactive at rat A1/A2a receptors.

89 13, displayed a Ki value of 0.59 nM at human A3 receptors and was moderately selective for that subty

90 antagonists of competitive binding at human A3 receptors, and K(i) values ranging from 120 nM to 101

91 , 3, which had a Ki value of 7.7 nM at human A3 receptors, and was 40- and 14-fold selective vs rat A

92 ethyluronamide (Cl-IB-MECA), and a selective A3 receptor antagonist, 3-ethyl-5-benzyl-2-methyl-4-phen

93 etabotropic glutamate receptor 1 (mGluR1) or A(3) receptor antagonists, indicating a role for both gl

94 levels after OGD was prevented by mGluR1 or A(3) receptor antagonists, indicating that AMPARs are de

95 potent as other recently reported, selective A(3) receptor antagonists; however, they display uniquel

96 ceptor antagonist CGS15943, but not by A1 or A3 receptor antagonists.

97 Adenosine A(3) receptors are of interest in the treatment of cardi

98 e signaling pathways activated by the A1 and A3 receptors are distinct and involve selective coupling

99 Thus, adenosine A1 and A3 receptors are linked to different G-proteins.

100 Since rodent adenosine A3 receptors are not blocked by theophylline, selective

101 he rat and human adenosine A1, A2A, A2B, and A3 receptors are presented.

102 Rodent A3 receptors are relatively insensitive to xanthines; in

103 upregulation; (2) the A2a, but not the A1 or A3, receptors are the major expressed and functionally c

104 adenosine receptors, but not A(2B), A(1), or A(3) receptors, are shown to be mostly responsible for e

105 peripheral blood eosinophils express the ADO A3 receptor as indicated by detection of the transcript

106 imidazo[2.1-i]pur in-5-one (PSB-11) from the A3 receptors, as well as [3H]N6-[(R)-phenylisopropyl]ade

107 ed the effects of an agonist in a functional A3 receptor assay, i.e. inhibition of adenylyl cyclase i

108 made synthetic ligands, we mutated the human A(3) receptor at the site of a critical His residue in T

109 ion constant (K(i)) value of 219 nM at human A(3) receptors (binding of [(125)I]AB-MECA (N(6)-(4-amin

110 ), may be substituted with L (present in the A3 receptor) but not with D (in biogenic amine receptors

111 ic and electrostatic regions with the A1 and A3 receptors, but not the A2A.

112 us, co-activation of both adenosine A(1) and A(3) receptors by the binary A(1)/A(3) agonists represen

113 nyl or 3-furyl group reduced the affinity at A3 receptors by 4- and 9-fold, respectively.

114 ding pyridine derivative reduced affinity at A3 receptors by 88-fold and slightly increased affinity

115 A novel adenosine A3 receptor can mediate this protective function.

116 Also, increased expression of the A3 receptor caused an enhanced cardioprotective effect b

117 cells with cDNA encoding the human adenosine A3 receptor causes a sustained A3 agonist-mediated cardi

118 y transfected with the human adenosine A1 or A3 receptor cDNA individually or they were cotransfected

119 ene transfer and overexpression of the human A3 receptor cDNA, renders the myocytes resistant to the

120 at least two populations of agonist-occupied A3-receptor complexes, showing different motilities with

121 and antagonists suggested that activation of A(3) receptors could induce mast cell histamine release

122 eness to aerosolized adenosine in wild-type, A(3) receptor-deficient, and mast cell-deficient mice.

123 ty at the H272E mutant relative to wild-type A(3) receptors, depending on the position of the amino g

124 with xanthines allows selective detection of A3 receptors despite the lack of selectivity of the liga

125 degree of selectivity for cloned human brain A3 receptors, determined in competitive binding assays v

126 rative interactions between protomers of the A(3)-receptor dimer in single living cells.

127 , and adenosine for the ABA-X-BY630-occupied A(3)-receptor dimer yielded values of 6.0 +/- 0.1, 5.9 +

128 ism combined with high functional potency at A(3) receptors (EC(50) < 1 nM) may produce tissue select

129 e protection mediated by prior activation of A3 receptors exhibits a significantly longer duration th

130 t of timing of hypertonic saline exposure on A3 receptor expression and degranulation was studied in

131 myl methionyl-leucyl-phenylalanine inhibited A3 receptor expression and degranulation, whereas hypert

132 l-leucyl-phenylalanine-stimulation augmented A3 receptor expression and degranulation.

133 Polymorphonuclear neutrophil A3 receptors expression determines whether hypertonic sa

134 ence that semaphorins, activating the Plexin-A3 receptor, function as retraction inducers to trigger-

135 ine-2,4-dione derivatives as human adenosine A3 receptor (hA3R) antagonists to determine their kineti

136 In the CA1 region, activation of A3 receptors had no direct effects on synaptically evoke

137 ding of flavonoids to adenosine A1, A2A, and A3 receptors has been conducted using comparative molecu

138 e renal tubular epithelium, A(1), A(2A), and A(3) receptors have all been identified as playing a rol

139 enosine receptor subtypes, A1, A2A, A2B, and A3 receptors, have been cloned and characterized.

140 At A1, A2A, and A3 receptors however the optimum occurs with four methyl

141 Activation of both endogenous A(1) and A(3) receptors in ventricular myocytes resulted in a pro

142 The function of A(3) receptors in vivo was tested by exposing mice to th

143 criminating hydrophobic region occurs in the A3 receptor in proximity to the N5-substituent.

144 pt that an increased expression of the human A3 receptor in the cardiac myocyte can be an important c

145 indicated by detection of the transcript for A3 receptors in polymerase chain reaction-amplified cDNA

146 d high specific activity, the low density of A3 receptors in rat brain appears insufficient to allow

147 ful for localization and characterization of A3 receptors in rat brain.

148 Therefore, involvement of ADO A3 receptors in the bronchoconstrictor and/or inflammato

149 eted using a rhodopsin-based model of ligand-A(3) receptor interactions.

150 The A3 receptor is coupled via RhoA to activate phospholipas

151 The adenosine A3 receptor is expressed in brain, but the consequences

152 ovides the first evidence that the adenosine A3 receptor is present on ventricular myocytes and can m

153 way, suggesting that selective activation of A3 receptors is an effective means of protecting the isc

154 Thus, activation of both A1 and A3 receptors is required to mediate the cardioprotective

155 confirm that adenosine, acting at A(2A) and A(3) receptors, is a potent regulator of inflammation.

156 e in radioligand binding assays for A(1) and A(3) receptors (K(i) values of 0.7-3.5 nm) versus A(2A)

157 selective (approximately 200-fold) for human A3 receptors (Ki = 0.56 microM).

158 wild-type mice, but not in those of A(2A) or A(3) receptor knockout mice.

159 in wild-type mice while having no effect in A(3) receptor knockout mice.

160 lammation in an air-pouch model in A(2A) and A(3) receptor knockout mice.

161 ertonic saline resuscitation was assessed in A3 receptor knockout and wild-type mice.

162 Mortality in A3 receptor knockout mice remained only 50% regardless o

163 ed hypertonic saline-treatment was absent in A3 receptor knockout mice.

164 onists that activate both adenosine A(1) and A(3) receptors may thus prove beneficial for the treatme

165 Here we investigated whether A3 receptors may diminish the efficacy of hypertonic sal

166 e affinity of flavones at both rat and human A3 receptors may explain some of the previously observed

167 y of neonatal mononuclear cells to adenosine A3 receptor-mediated accumulation of cAMP, a second mess

168 ominant negative RhoA (RhoAT19N) blocked the A3 receptor-mediated phospholipase D activation and card

169 I870R preferentially inhibited the human A3 receptor-mediated protection from ischemia.

170 The study indicates that cardiac adenosine A3 receptor mediates a sustained cardioprotective functi

171 s as TNF-alpha inhibitors suggested that the A3 receptor might be involved (N6-(3-iodobenzyl)-9-[5-(m

172 hypothesis, using a previously derived human A(3) receptor model, shows the bulkier of the two ester

173 uced by coexpression of a nonbinding (N250A) A(3)-receptor mutant.

174 the (S)-analogue, particularly at the human A(3) receptor (N/S affinity ratio of 150).

175 In binding assays at A(1), A(2A), and A(3) receptors, (N)-methanocarba-adenosine was of higher

176 -356 nM), and heteromeric GluA1/A2 and GluA2/A3 receptors nonselectively, with IC(50) values in the m

177 A3 receptors on eosinophil membranes were characterized

178 These results attest to the existence of ADO A3 receptors on eosinophils and suggest that ADO stimula

179 The effect of A3 receptors on the efficacy of hypertonic saline resusc

180 Moreover, activation of A(2b)/A(3) receptors or activation of PKCepsilon prevented deg

181 n the dissociation kinetics of 125I-ABA from A3 receptors or [125I]-[2-(4-amino-3-iodo-phenyl)ethylam

182 r cells expressing native adenosine A(1) and A(3) receptors, or engineered atrial cells, in which eit

183 The specificity of the A(3) receptor-phospholipase D interaction was also demon

184 Activation of adenosine A1 or A3 receptors protects heart cells from ischemia-induced

185 ease and autocrine feedback through P2Y2 and A3 receptors provide signal amplification, controlling g

186 by > 95%, indicating that xanthine-resistant A3 receptors represent a quantitatively minor subtype.

187 uman A(2B) receptors versus human A(1)/A(2A)/A(3) receptors, respectively, and 8.5- and 310-fold sele

188 ivative had K(i) values of 4.1 and 2.2 nM at A(3) receptors, respectively, and were highly selective

189 pounds are potent agonists at either A(1) or A(3) receptors, respectively, were synthesized.

190 Ki values of 41.3 and 1.90 microM at A1 and A3 receptors, respectively, and was inactive at A2A rece

191 hich was less potent than 27 at A1, A2A, and A3 receptors, retained moderate potency at A2B receptors

192 ibution of neural adenosine A1, A2a, A2b, or A3 receptors (Rs) in the human intestine was investigate

193 of the 6-phenyl substituent was tolerated in A3 receptor selective agents.

194 The adenosine A3 receptor-selective antagonist 3-ethyl 5-benzyl-2-meth

195 Inclusion of a 6-phenyl group enhanced A3 receptor selectivity: Compound 28 (MRS1097; 3,5-dieth

196 These data suggest that A(3) receptor signaling is key to adenosine-mediated STA

197 The A3 receptor signals via RhoA and phospholipase D (PLD) t

198 ine (BW-A1433), an antagonist of A1, A2, and A3 receptors, significantly reduced the vasoconstrictor

199 binary agonist MRS 1741 coactivated A(1) and A(3) receptors simultaneously, with full cardioprotectio

200 silon and ALDH2 were both activated by A(2b)/A(3) receptor stimulation in HMC-1, and PKCepsilon inhib

201 Further, RAW 264.7 A(3) receptor stimulation with Cl-IB-MECA reduces IFN-ga

202 each being selective for either the A(1) or A(3) receptor subtype.

203 eceptors with particular selectivity for the A3 receptor subtype.

204 led in myocytes cotransfected with the human A3 receptor than in those cells expressing the human A1

205 3-keto derivative was 5-fold more potent at A3 receptors than a related open-ring analogue.

206 ne ring, esters were much more selective for A3 receptors than closely related thioester, amide, and

207 al myocytes (which do not express endogenous A(3) receptors) that had been transfected with a vector

208 At the A(3) receptor, this could be markedly increased by both

209 A3 receptor transcript was substantially diminished, and

210 ogue was shown to increase affinity at human A(3) receptors upon oxidation from the 1-methyl-1,4-dihy

211 was determined at cloned human and rat brain A3 receptors using [125I]-AB-MECA [N6-(4-amino-3-iodoben

212 Affinity was determined at cloned human A3 receptors using [125I]AB-MECA (N6-(4-amino-3-iodobenz

213 inity was determined at cloned human and rat A3 receptors using [125I]AB-MECA [N6-(4-amino-3-iodobenz

214 inity was determined at cloned human and rat A3 receptors using [125I]AB-MECA [N6-(4-amino-3-iodobenz

215 one visnagin was 30-fold selective for human A3 receptors vs either rat A1 or A2A receptors.

216 o bind with 14-17-fold selectivity for human A3 receptors vs rat A1 and A2A receptors, with a Ki valu

217 A reduction in XAC potency at the A(1) and A(3) receptor was achieved within 1 min of Brilliant Bla

218 ngener (XAC) and XAC-X-BY630 at the A(1) and A(3) receptors was significantly decreased in the presen

219 A rhodopsin-based model of the human A3 receptor was built, and the pyridine reference ligand

220 umulation in intact cells that express human A3 receptors was employed as a functional index of A3 re

221 ioligand binding by BTH4 (7) at cloned human A3 receptors was negligible but one slightly A3 selectiv

222 , whereas messenger RNA expression of A1 and A3 receptors was reduced (both, p = .03).

223 erivative, 26, with a Ki value of 58.3 nM at A3 receptors, was > 1700-fold selective vs either A1 rec

224 tive, 24, with a Ki value of 0.670 microM at A3 receptors, was 24-fold selective vs A1 receptors (Ki

225 rate constants of ABA-X-BY630 from A(1) and A(3) receptors were 1.45 +/- 0.05 and 0.57 +/- 0.07 min(

226 s having mixed selectivity for both A(1) and A(3) receptors were created through the covalent linking

227 A(3) receptors alone or both human A(1) and A(3) receptors were expressed.

228 oned media was maximal if both HMC-1 A2B and A3 receptors were activated, whereas activation of A2B r

229 and A(2B) adenosine receptors but not in the A(3) receptor, which is cerebroprotective and cardioprot

230 cover a signaling cascade initiated by A(2b)/A(3) receptors, which triggers PKCepsilon-mediated ALDH2

231 Inhibition of the adenosine A(3) receptor with a subtype-specific antagonist (MRS 11

232 f the adenosine A1 receptor with CCPA or the A3 receptor with C1-IB-MECA can replace preconditioning

233 However, activation of A3 receptors with Cl-IB-MECA antagonized the adenosine A

234 quinazolin-5-amine (CGS15943) binds to human A3 receptors with high affinity (Ki = 14 nM), while it l

235 ) binds nonselectively to human A1, A2A, and A3 receptors with high affinity.

236 lectron-withdrawing groups were specific for A3 receptors with nanomolar Ki values and selectivity as

237 derivative was the most potent derivative at A3 receptors, with a Ki value of 0.36 nM.

238 carboxylate , 38, was highly potent at human A3 receptors, with a Ki value of 20 nM.

239 tive and highly potent at both human and rat A3 receptors, with Ki values of 18.9 and 113 nM, respect