ライフサイエンスコーパス: A(2B) receptor

1 tential mediator of angiogenesis through the A2B receptor.

2 eptor other than A1, A2A or A3, possibly the A2B receptor.

3 cutely isolated astrocytes is coupled to the A2B receptor.

4 t the effect is likely to be mediated by the A2b receptor.

5 olving adenosine signaling via the adenosine A2b receptor.

6 receptors and HMEC-1 preferentially express A2B receptors.

7 xanthine 3 was >13-fold more potent at human A2B receptors.

8 a pA2 value of 8.0 but was not selective for A2B receptors.

9 d A3 receptors, retained moderate potency at A2B receptors.

10 c fibroblast proliferation via activation of A2B receptors.

11 A2A receptors and suggested a major role for A2B receptors.

12 euromodulator adenosine acting on astrocytic A2B receptors.

13 which was prevented by blockade of adenosine A2B receptors.

14 message and protein expression of A(2A) and A(2B) receptor.

15 xy derivative 9 was moderately selective for A(2B) receptors.

16 and A(2A) receptors and at recombinant human A(2B) receptors.

17 enosine T1 is mediated through the A(2A) and A(2B) receptors, (2) adenosine myocardial perfusion rese

18 n contrast, AMP only activated the adenosine A(2B) receptor (A(2B)R) after hydrolysis to adenosine by

19 The human adenosine A(2B) receptor (A(2B)R) is a class A G protein-coupled r

20 ed adenosine functions through the adenosine A(2B) receptor (A(2B)R) to activate the PI3K/AKT signali

21 logical approaches, we showed that adenosine A(2B) receptor (A(2B)R)-mediated induction of 2,3-diphos

22 -tertiary butyl phenol was identified as the A2b receptor (a P1 receptor for adenosine).

23 Adenosine acts through the A2b receptor, a G protein-coupled receptor that couples

24 y of p73 to upregulate the expression of the A2B receptor, a recently characterized p53 target that e

25 ating selective induction of human adenosine A2B receptor (A2BR) by hypoxia.

26 On binding ADO, the A2B receptor (A2BR) stimulates cAMP production to activa

27 After myocardial infarction, A2b receptor (A2bR) transcription was induced in both T

28 Acting through the adenosine A2b receptor (A2bR), the luminally derived adenosine ind

29 These results indicate that A(2B) receptor activation may offer a new therapeutic ap

30 A(2B) receptor activation promotes the inflammatory resp

31 ular permeability occurred through adenosine A2B receptor activation and was accompanied by a paralle

32 Because luminal A2B receptor activation does not raise total cellular cA

33 g of axon growth and guidance independent of A2B receptor activation.

34 ed ecto-5'-nucleotidase (CD73) and adenosine A(2B) receptor (ADORA2B) in the placentas of PE mouse mo

35 roarray analysis revealed that the adenosine A2B receptor (AdoRA2B) is selectively up-regulated by hy

36 signaling through the erythrocyte adenosine A2B receptor (ADORA2B) promotes O2 release to counteract

37 The A2B receptor affinity-enhancing effects of 7-(2-chloroet

38 ormalized by pretreatment with the selective A(2B) receptor agonist BAY 60-6583.

39 the adenosine receptor agonist NECA and the A2B receptor agonist BAY60-6583.

40 hese results suggest that the development of A(2B) receptor agonists to induce vasodilatation in the

41 The work suggests that adenosine A2B receptor agonists and inhibition of equilibrative nu

42 Cyclic AMP elevators and adenosine A2b receptor agonists rejuvenated the behavior of old gr

43 eptors were activated, whereas activation of A2B receptor alone was less effective.

44 s evidence of anti-inflammatory functions of A(2B) receptors and it was suggested that antagonists wi

45 inflammatory role of adenosine signaling via A(2B) receptors and the anti-inflammatory actions of A(2

46 ing pathway: both treatments act through the A2b receptor and specifically activate the Epac1/RapGef3

47 was impaired, with a lower expression of the A2B receptor and the cAMP-response element binding prote

48 reduces bladder contractility by activating A2B receptors and large-conductance calcium-activated po

49 ol-induced hepatic steatosis via both A1 and A2B receptors and suggest that targeting adenosine recep

50 /IL3 signaling, is mediated by the adenosine A(2B) receptor, and can be pharmacologically reversed.

51 human mast cell line HMC-1 expresses A2A and A2B receptors, and that both receptors activate adenylat

52 ation of intracellular Ca(2+) inhibited both A(2B) receptor- and ionomycin-dependent IL-4 secretion.

53 A(2B) receptor antagonism may be an effective treatment

54 was blocked by adenosine A2A, but not A1 or A2B, receptor antagonism.

55 ne mimicked the effect of MTX, and adenosine A2b receptor antagonist (3,7-dimethyl-1-propargylxanthin

56 The A2B receptor antagonist alloxazine, however, was able to

57 effect of NECA was reversed by the selective A2B receptor antagonist N-(4-cyanophenyl)-2-[4-(2,3,6,7-

58 ar accumulation, which were inhibited by the A2B receptor antagonist PSB603 [(8-[4-[4-((4-chlorophenz

59 2A receptor antagonist), but not by MRS1754 (A2B receptor antagonist), and it was mimicked by the A2A

60 mice treated with either an adenosine A1 or A2B receptor antagonist.

61 mately 50% with combined adenosine A(2a) and A(2b) receptor antagonists and completely abolished by a

62 report the synthesis of potent and selective A(2B) receptor antagonists.

63 Neither A1, A2A, nor A2B receptor antagonists affected the capacity of MTX to

64 tial therapeutic implications given that A2A/A2B receptor antagonists have already entered clinical t

65 In this study, we revealed that A2A/A2B receptor antagonists were effective in reducing the

66 cked by theophylline, selective A1, A2A, and A2B receptor antagonists were tested as well.

67 together, these data indicate that A(2A) and A(2B) receptors are regionally selective in their regula

68 A(2B) receptors are, thus, potentially important pharmac

69 enylate cyclase via Gs-protein but that only A2B receptors are also coupled to phospholipase C via Gq

70 al cancer (DCC), neogenin, and the adenosine A2b receptor] are expressed by the fetal mucosal epithel

71 adenosine receptor knockout mice identified A(2B) receptor as the mediator of adenosine effects on D

72 Furthermore, we identify the A2b receptor as a central player in this process.

73 These data identify the adenosine A2B receptor as an astrocytic sensor of neuronal activit

74 the 3-position favored affinity at the human A2B receptor, as indicated by 1-allyl-3-methyl-8-phenylx

75 This effect was mediated by A(2B) receptors because neither the selective A(2A) agon

76 atory effect of adenosine required primarily A(2B) receptors because the nonselective adenosine recep

77 on IL-10 production was mediated through the A(2B) receptor, because the order of potency of selectiv

78 that an electron-rich ring was preferred for A2B receptor binding.

79 Combining IDO1 inhibition and A2a/A2b receptor blockade improved survival and boosted the

80 a treatment also increased the expression of A(2B) receptors, but decreased expression of A(2A) recep

81 a luciferase reporter in HMEC-1 showed that A2B receptors, but not A1, A2A, or A3, activated IL-8 an

82 athophysiological conditions, the purinergic A2b receptor can regulate cell motility, but the underly

83 er ovary cells stably transfected with human A2B receptor cDNA, inhibition of agonist-induced cyclic

84 A molecular model of the 27-A2B receptor complex based on the structure of rhodopsin

85 ective antagonists of both adenosine A2A and A2B receptors, consistent with ligation of these recepto

86 Both A(2A) and A(2B) receptors couple to G(s) proteins and stimulate ad

87 e on their luminal surface through adenosine A2B receptors coupled to adenylyl cyclase.

88 ble for the increased inflammation of septic A(2B) receptor-deficient mice.

89 nuclear factor of activated T cells, because A(2B) receptor-dependent IL-4 secretion was blocked with

90 ylate cyclase or protein kinase A attenuated A(2B) receptor-dependent IL-4 secretion.

91 on of phospholipase Cbeta completely blocked A(2B) receptor-dependent IL-4 secretion.

92 G(s)-linked pathways also play a role in the A(2B) receptor-dependent stimulation of IL-4 secretion;

93 ntracellular signaling, we demonstrated that A2B receptor-dependent accumulation of JunB protein and

94 PK pathways are essential steps in adenosine A2B receptor-dependent stimulation of IL-8 production in

95 s, our data suggest an important role of the A2B receptor-dependent upregulation of JunB in VEGF prod

96 Mice lacking the A2b receptor display increased sensitivity to IgE-mediat

97 of extracellular adenosine or inhibition of A2B receptors enhanced pro-fibrotic ATP signaling.

98 Knockdown of A2B receptor expression in astrocytes led to a major rep

99 hrough activation of PMN adenosine A(2A) and A(2B) receptors, functions as an antiadhesive signal for

100 tative trait locus upstream of the adenosine-A2B receptor gene (ADORA2B).

101 Genetic ablation of A(2B) receptors had no effect on A(3) adenosine receptor

102 on by E coli-challenged macrophages, whereas A(2B) receptors have a minor role.

103 cyano, and acetyl, bind selectively to human A(2B) receptors in the range of 1-3 nM.

104 To better understand the regulation of the A2b receptor in intestinal epithelia, we studied the eff

105 report increased expression of the adenosine A2b receptor in meniscus cells after stimulation at the

106 and provide further support for the role of A2B receptor in retinal angiogenesis.

107 ng conditional deletion of the gene encoding A2B receptors in astrocytes showed that adenosine-mediat

108 rs in promoting fatty acid synthesis and for A2B receptors in decreasing fatty acid metabolism.

109 adenosine agonist compounds for the A2A and A2B receptors in human cells.

110 Genetic deficiency of A(2B) receptors increased the mortality of mice sufferin

111 The lack of a potent, selective A2B receptor inhibitor has hampered its characterization

112 The A(2B) receptor is a likely target of CD73-generated aden

113 Adenosine signaling through A(2B) receptor is an important factor of aberrant DC dif

114 lial dependent while T1 mediated through the A(2B) receptor is endothelial independent.

115 otective effects of HPC are negated when the A2B receptor is nonfunctional, the hypoxia-->adenosine--

116 enal perfusion by endothelial cell adenosine A2B receptors is antagonized by adenosine reuptake into

117 While involvement of A2B receptors is not excluded, adenosine may activate af

118 In addition, A(2B) receptor knockout mice showed increased splenic ap

119 receptor knockout), A(2B)AR(-/-) (adenosine A(2B) receptor knockout), A(3)AR(-/-) (adenosine A(3) re

120 f Sca-1(+)CD31(-) cells generated from WT or A2B receptor knockout (A2BKO) mice or the same volume of

121 s much milder than we previously reported in A2b receptor knockout (A2bKO) mice, suggesting compensat

122 s bladder activity through the activation of A2B receptors, linking acute hypoxia to bladder relaxati

123 A2B receptors mediate VEGF and IL-8 secretion because ne

124 , CAF-CD73 expression is enhanced via an ADO-A(2B) receptor-mediated feedforward circuit triggered by

125 3-yl)maleimide (Ro-32-0432) had no effect on A(2B) receptor-mediated IL-4 secretion but inhibited pho

126 ther apical or basolateral adenosine induces A2b receptor-mediated increase in IL-6 secretion, which

127 indings demonstrate that inosine acts via an A2B receptor-mediated pathway that impinges on specific

128 phenyl)-5-(4-pyridyl)1H- imidaz ole) blocked A2B receptor-mediated production of IL-8.

129 A2a and A2b receptor messenger RNA expression was elevated (p =

130 n experiments with A(2A)AR(-/-) or adenosine A(2B) receptor(-/-) mice, the effect of AMO injection wa

131 ribozyme that would specifically cleave the A2B receptor mRNA and examine its effect on retinal angi

132 the plasmid expressing the ribozyme reduced A2B receptor mRNA levels by 45+/-4.8% (P=5.1x10(-5)).

133 lls were transfected with these plasmids and A2B receptor mRNA levels were determined by quantitative

134 Ribozymes specific for the mouse and human A2B receptor mRNAs were designed and cloned in expressio

135 A1, A2A, A3, and barely detectable levels of A2B receptor mRNAs.

136 unsubstituted anilide 12 had a K(i) value at A(2B) receptors of 1.48 nM but was only moderately selec

137 s of adenosine in tumors activates A(2A) and A(2B) receptors on immune cells and inhibits their abili

138 row chimeras revealed that it is the lack of A(2B) receptors on nonhematopoietic cells that is primar

139 Stimulation of the A2b receptor on FLS decreases collagenase gene expressio

140 DNA transfection, we also developed A2A and A2B receptor over-expressing lines.

141 is nonfunctional, the hypoxia-->adenosine-->A2B receptor pathway plays a critical role in the preven

142 suppresses bladder contractility through the A2B receptor pathway.

143 Although A2B receptors play a major role in the regulation of BR

144 In colonic epithelium the A(2B) receptor plays a prominent role in regulating Cl(-

145 as recently been proposed that the adenosine A2B receptor plays a crucial role in skeletal muscle ene

146 A2B receptors, predominantly expressed in human microvas

147 d both pharmacologic and genetic blockade of A(2B) receptors prevented the effect of NECA.

148 Activation of the adenosine A2B receptor, proposed to contribute to netrin effects o

149 we demonstrate that genetic ablation of the A(2B) receptor protein has two distinct effects on BMMCs

150 Stimulation of A2B receptors recruits the canonical cyclic adenosine 3'

151 Activation of the A2b receptor results in cyclic AMP-dependent activation

152 by this process activates surface adenosine A(2B) receptors, results in endothelial junctional reorg

153 Our results suggest that the A2B receptor ribozyme will provide a tool for the select

154 By Western blotting, the H/F-A(2B) receptor runs as a 34.8-kDa glycoprotein.

155 ituted in the 1-, 3-, 7-, and 8-positions as A2B receptor-selective antagonists have been identified.

156 ogenous adenosine deaminase, suggesting that A(2b) receptors sense endogenous adenosine within the AS

157 in expression or membrane recruitment of the A2b receptor, shown to be essential for its function.

158 actors, we hypothesized that ablation of the A2B receptor signaling in these cells would reduce their

159 Thus, our study demonstrated that the A2B receptor signaling linked to up-regulation of pro-an

160 adenosine, which in turn promotes adenosine-A2b receptor signaling to relax bladder smooth muscle (B

161 sine agonist, the desensitization of A2a and A2b receptor-stimulated adenylyl cyclase in dominant neg

162 lls, the rates of desensitization of A2a and A2b receptor-stimulated adenylyl cyclase were markedly s

163 A(2B) receptor stimulation also promotes the production

164 A(2B) receptor stimulation limits endothelial cell infla

165 timulation predominantly mediated by the Ado A2B receptor subtype.

166 yR a2 subunit which results in a heteromeric a2B receptor that is insensitive to ethanol.

167 oalkylacyl derivatives demonstrated that for A2B receptors the optimal chain length occurs with three

168 signal in a paracrine faction ciliated cell A(2b) receptors to activate ion/water secretion and appr

169 racellular pathways that link stimulation of A(2B) receptors to IL-4 up-regulation in HMC-1 mast cell

170 Caco2-BBE cells stably transfected with GFP-A2b receptor to study the intestinal A2bR.

171 ses (PDEs) confines cAMP generated by apical A2B receptors to a microdomain that includes the CFTR ch

172 product of ATP hydrolysis by ENTPD, acts via A2B receptors to counterbalance the pro-fibrotic respons

173 ion of phospholipase C indicated coupling of A2B receptors to G(q) proteins in HMEC-1.

174 Additionally, A(2B) receptor transcript expression was not affected by

175 In LLC cells expressing A2A and A2B receptor transcripts, only the nonselective adenosin

176 We conclude that A(2B) receptors up-regulate IL-4 through G(q) signaling

177 Both forskolin and stimulation of A(2B) receptors up-regulated NFATc1 protein levels.

178 current study, we tested the hypothesis that A2B receptors upregulate JunB, which can contribute to s

179 400-, 245-, and 123-fold selective for human A(2B) receptors versus human A(1)/A(2A)/A(3) receptors,

180 receptor muscarinic 3), purinergic P2X1, and A2b receptors was unchanged, whereas P2Y12 receptor was

181 ous series, maintaining the potency at human A(2B) receptor, was achieved, as exemplified by the 8-[3

182 tage for selectivity, and high affinities at A(2B) receptors were maintained.

183 king ecto-5'-nucleotidase or adenosine A1 or A2B receptors were protected from developing fatty liver

184 naling is achieved through adenosine A2A and A2B receptors, which are Gs coupled, and their activatio

185 ides with acrylic acid decreased affinity at A(2B) receptors while increasing affinity at A(1) recept

186 osine A2A receptor; 12-fold versus adenosine A2B receptor) with improved oral efficacy in the rat diu