ライフサイエンスコーパス: P2 receptor

1 ndicating the mediatory role of a purinergic P2 receptor.

2 these two cell populations express different P2 receptors.

3 functionalities known to enhance potency at P2 receptors.

4 as previously unreported agonist activity at P2 receptors.

5 orm a bisphosphate, which reduced potency at P2 receptors.

6 e on the phenylazo ring modulated potency at P2 receptors.

7 not stem from activation of volume-sensitive P2 receptors.

8 ith molecular species other than ATP-binding P2 receptors.

9 cellular ATP acts directly on bone cells via P2 receptors.

10 olecule through the activation of purinergic P2 receptors.

11 ecto-ATPase and by suramin, an antagonist of P2 receptors.

12 ening of Cl- channels through stimulation of P2 receptors.

13 ological activities by activating purinergic P2 receptors.

14 lar ATP by way of the activation of specific P2 receptors.

15 crovascular EC through actions on purinergic P2 receptors.

16 nstrated that keratinocytes express multiple P2 receptors.

17 mate, serotonergic (5-HT(3)) and purinergic (P2) receptors.

18 cellular nucleotides acting through specific P2 receptors activate intracellular signaling cascades.

19 propose that CD39 deficiency and changes in P2 receptor activation abrogate secretion of interferon

20 ith ecto-5'-nucleotidase, not only terminate P2 receptor activation and trigger adenosine receptors b

21 interferon gamma secretion are inhibited by P2 receptor activation in vitro.

22 We examined the effect of P2 receptor activation on voltage-gated ionic currents i

23 ase from the epithelial cells and successive P2 receptor activation.

24 e to bacterial challenge by enhancing P1 and P2 receptor activation.

25 r was caused by low doses of the nonspecific P2 receptor agonist ATP, the P2Y2 receptor agonist UTP (

26 The mucosal epithelial surface eliminated P2 receptor agonists (ATP = UTP > ADP > UDP) at 3-fold h

27 The P2 receptor agonists alpha,beta-methylene ATP, adenosine

28 P, and other nucleotides and nonhydrolyzable P2 receptor agonists and antagonists suggests that ATP r

29 nerve fibers is increased by the presence of P2 receptor agonists at the peripheral nerve ending and

30 P2 receptor agonists induced salivation in an ex vivo su

31 bitor ARL67156, and exogenous nucleotides or P2 receptor agonists on DBS.

32 P2 receptor agonists stimulated both the cation current

33 nd UTP, and we compared the effects of these P2 receptor agonists with those of growth factors and ot

34 ere we discuss how signalling events through P2 receptors alter the outcomes of inflammatory or infec

35 elling elicits ATP release, which stimulates P2 receptors and activates Cl(-) channels, and that this

36 We hypothesize that P2 receptors and adenosine transporters could be novel t

37 hibitory effects of antagonists of mammalian P2 receptors and calcium influx inhibitors on nucleotide

38 ed via nucleotides (ATP, UTP) binding apical P2 receptors and increasing [Ca(2+)](i).

39 des increase proliferation via activation of P2 receptors and induction of calcium transients, while

40 ighly selective (IC50 >10 microM) over other P2 receptors and other neurotransmitter receptors, ion c

41 toma cells transfected to express individual P2 receptors and/or the gap junction protein connexin43.

42 i) ATP efflux, (ii) autocrine stimulation of P2 receptors, and (iii) increases in anion permeability

43 ists at the family of receptors known as the P2 receptors, and in keratinocytes the P2Y2 subtype is k

44 intracellular Ca(2+) concentration, whereas P2 receptor antagonism blocked DOR stimulation of inosit

45 nical strain and was completely blocked by a P2 receptor antagonist and by inhibition of p38/mitogen-

46 Attenuation of this response by the P2 receptor antagonist PPADS suggests that bradykinin-in

47 Novel analogues of the P2 receptor antagonist pyridoxal-5'-phosphate 6-azopheny

48 ATP receptors in the VLM (microinjection of P2 receptor antagonist pyridoxal-5'-phosphate-6-azopheny

49 and hP2X(2b) receptors were sensitive to the P2 receptor antagonist pyridoxal-5-phosphate-6-azophenyl

50 agal neurons which were blocked by the broad P2 receptor antagonist pyridoxal-phosphate-6-azophenyl-2

51 agal neurons which were blocked by the broad P2 receptor antagonist pyridoxal-phosphate-6-azophenyl-2

52 lphabetam-ATP were blocked completely by the P2 receptor antagonist pyridoxalphosphate-6-azophenyl-2'

53 P2 receptor antagonist studies indicated a role for P2X2

54 These were blocked by the P2 receptor antagonist suramin (100 microm).

55 The P2 receptor antagonist suramin inhibited these intercell

56 lement pathway Ab eculizumab, the purinergic P2 receptor antagonist suramin, and EDTA.

57 ntagonist oxidized ATP (oATP) but not by the P2 receptor antagonist suramin; both ATP and BzATP incre

58 In the isolated retina, suramin (P2 receptor antagonist) reduces the frequency of spontan

59 gent of ADP degradation), suramin (a general P2 receptor antagonist), pyridoxal 5'-phosphonucleotide

60 Suramin, a nonselective P2 receptor antagonist, and MRS-2179, a P2Y1 receptor-se

61 Suramin (500 mum), a broad-spectrum P2 receptor antagonist, dilated retinal arterioles by 50

62 sly we have shown that injection of PPADS, a P2 receptor antagonist, into the arterial supply of skel

63 sion of GFAP and MMP-9 and a purinergic ATP (P2) receptor antagonist reduction in calcium response id

64 In the presence of the P2-receptor antagonist suramin (0.1 mM), the amplitude o

65 ist sulfonylphenyl theophylline, but not the P2-receptor antagonist suramin, antagonized the effect o

66 In the presence of P2 receptor antagonists A2P5P or AR-C67085, LIBS6 failed

67 terms of insensitivity to blockade by known P2 receptor antagonists and the ineffectiveness of adeno

68 However, treatment with P2 receptor antagonists did not alter the ratio of nesti

69 n, and the acyclic approach to the design of P2 receptor antagonists is valid.

70 P2 receptor antagonists or P2Y(6) antisense oligonucleot

71 Similarly, P2 receptor antagonists or SC49992 blocked ADP-induced a

72 L67156 and were depressed in the presence of P2 receptor antagonists PPADS (10 microm) and suramin (5

73 Analogues of the P2 receptor antagonists pyridoxal-5'-phosphate and the 6

74 s blocked by ionophoretic application of the P2 receptor antagonists suramin (0.02 M) and pyridoxal-p

75 0.1-30 micrometer) and were sensitive to the P2 receptor antagonists suramin and iso-PPADS.

76 The P2 receptor antagonists suramin and pyridoxalphosphate-6

77 These effects were blocked by the P2 receptor antagonists XAMR 0721, periodate-oxidized AT

78 Pretreatment of astrocytes with P2 receptor antagonists, including suramin and periodate

79 ve antagonist, MRS2179, and the nonselective P2 receptor antagonists, pyridoxal phosphate 6-azophenyl

80 ed by apyrase inactivation of nucleotidases, P2 receptor antagonists, tetrodotoxin (TTX), or piroxica

81 (2+)]i oscillations, which were abolished by P2 receptor antagonists.

82 reduced or abolished by prior application of P2 receptor antagonists.

83 dently reduced in the presence of ATPases or P2 receptor antagonists.

84 l CO2/H+ sensitivity by an amount similar to P2 receptor antagonists.

85 ng expansion, and were reversibly blocked by P2 receptor antagonists.

86 n the absence of factor B, and by purinergic P2 receptor antagonists.

87 Activation of P2 receptors appears to influence endothelial cell chemo

88 P2 receptors are expressed during muscle development, an

89 Since P2 receptors are generally coupled to Ca(2+) signaling p

90 hat ATP release and activation of purinergic P2 receptors are involved in melittin-induced ADAM activ

91 bilization and support the idea that several P2 receptors are involved in the regulation of different

92 Nucleotides, acting as agonists at P2 receptors, are important extracellular signaling mole

93 Type 2 purinergic (P2) receptors bind extracellular nucleotides and are exp

94 es of respiratory neurone and the effects of P2 receptor blockade on CO2-evoked changes in activity i

95 P, the CO2-evoked effects were unaffected by P2 receptor blockade.

96 y focal ATP application; however, purinergic P2-receptor blockade did not affect their CO2/H(+) respo

97 tive raphe neurons were unaffected by ATP or P2-receptor blockade.

98 These effects were abolished by the P2 receptor blocker suramin (0.02 M, 80 nA), which also

99 ificantly less sensitive to the nonselective P2 receptor blocker suramin than the UTP-mediated increa

100 hate-6-azophenyl-2',4'-disulfonate (PPADS, a P2 receptor blocker) decreased the ventilatory response

101 Injections of ATP or a P2-receptor blocker into the medullary raphe had no effe

102 espiratory activity; however, injection of a P2-receptor blocker into this region had no effect on ba

103 -patch recordings from RTN neurons show that P2 receptor blockers decreased responsiveness to both 10

104 e apyrase (3 units/ml) or by exposure to the P2 receptor blockers suramin and Reactive Blue 2 (10-100

105 s much data to suggest roles for presynaptic P2 receptors but little to demonstrate which specific re

106 inflammation by acting on type 2 purinergic (P2) receptors, but the role of CD39 and CD39(+) Tregs in

107 Activation of a purinergic P2 receptor by adenosine 5'-triphosphate (ATP) has previ

108 singly recognized that stimulation of apical P2 receptors can influence solute transport in the nephr

109 ophs, and that these actions are mediated by P2 receptor channels.

110 we could assess the indomethacin-insensitive P2 receptor component.

111 These data suggest that P2 receptors contribute to the exercise pressor reflex i

112 through the interaction of nucleotides with P2 receptors, controls multiple biological responses.

113 xtracellular nucleotides, signalling through P2 receptors, could play an important role in modulating

114 ase and autocrine stimulation of purinergic (P2) receptors couple increases in cell volume to opening

115 s, thereby modulating the type-2 purinergic (P2) receptors demonstrated on these cells.

116 increased breathing and blood pressure by a P2-receptor-dependent mechanism.

117 Cs showed ATP unresponsiveness (secondary to P2-receptor desensitization) and impaired antigen-presen

118 ative and provide a potential new avenue for P2 receptor drug development.

119 We have applied P2 receptor drugs to rat pial arterioles and measured ch

120 Blockage of P2 receptors eliminated the effect of ATP on the OHC ele

121 tors in the microenvironment, and pattern of P2 receptor engagement.

122 xternal stimuli, ionotropic and metabotropic P2 receptors, exo- and ecto-nucleotidases, second messen

123 The effect of these PGs on P2 receptors expressed in murine and human macrophages w

124 s physiological responses through purinergic P2 receptors expressed in the plasma membrane of virtual

125 ut significant differences in the pattern of P2 receptor expression in mice and humans confer the div

126 Here, we investigate P2 receptor expression in primary human monocyte-derived

127 , with a selectivity for that subtype of the P2 receptor family of >1000-fold.

128 itions and act as ligands for members of the P2 receptor family.

129 ceptors, filling a long-standing need in the P2 receptor field, and are also important lead compounds

130 classified as P1 receptors for adenosine or P2 receptors for ATP.

131 is and pharmacological profile of purinergic P2 receptors for extracellular nucleotides suggest that

132 ils are known to express several subtypes of P2 receptors for extracellular nucleotides, their functi

133 nities for specifically targeting individual P2 receptors for the treatment of inflammatory or infect

134 Signaling by purinergic P2 receptors has previously been linked to the antimycob

135 block Ca2+ entry induced by occupancy of the P2 receptor in two prostate cancer cell lines and inhibi

136 ferentially activates P2Y2 relative to other P2 receptors in MDCK-D1 cells (P2Y1 and P2Y11, as shown

137 There is also evidence that ATP may activate P2 receptors in preglomerular vessels, which may contrib

138 Consistent with the role of P2 receptors in signaling and secretion, the actions of

139 The role of P2 receptors in synaptic transmission to the rat medial

140 their regulation by basolateral and luminal P2 receptors in the duct.

141 ruli that receive input from ORNs expressing P2 receptors in the P2-internal ribosome entry site-tau-

142 he effect of antagonizing, or desensitizing, P2 receptors in the retrofacial area of the ventrolatera

143 processes through activation of nucleotide (P2) receptors in the plasma membrane.

144 TP; scavenging endogenous ATP and inhibiting P2 receptors, in the absence of other stimuli, rapidly i

145 The P2 receptors, including P2X and P2Y purinoceptor subtype

146 h kinetics revealed downregulation of select P2 receptors, including P2Y2R, in slow-growing hCPCs com

147 he soluble ecto-nucleotidase apyrase and the P2 receptor inhibitor suramin.

148 P2 receptor inhibitors, including oxidized ATP, blocked

149 Nucleotide activation of P2 receptors is important in autocrine and paracrine reg

150 in human astrocytes, and that signaling via P2 receptors may fine-tune the transcription of genes in

151 Therefore, aberrant regulation of nucleotide P2 receptors may influence angiogenesis in cd39-null mic

152 leotides, such as ATP and UTP, signaling via P2 receptors may provide a mechanism whereby cells can s

153 Although P2 receptors mediate a myriad of physiological effects o

154 that in primary human fetal astrocytes, the P2 receptor-mediated and gap junction-mediated pathways

155 (50 microg/kg per min), to avoid endothelial P2 receptor-mediated effects on nitric oxide release cau

156 rsely, transmission of calcium waves via the P2 receptor-mediated pathway was potentiated in IL-1beta

157 ction-mediated pathway and an extracellular, P2 receptor-mediated pathway, which link the cells into

158 From these data, we conclude that P2 receptor-mediated signaling intersects with that of I

159 lease waves, local ejection of ATP triggered P2 receptor-mediated waves that were refractory to repea

160 Nucleotides exert these functions via P2-receptor-mediated mechanisms that can also interact w

161 Adenosine triphosphate (ATP) acting at P2 receptors mediates some fast excitatory postsynaptic

162 The P2 receptor mediating the antiapoptotic actions of ATP w

163 low (via shear stress) or hypoxia, to act on P2 receptors on endothelial cells to produce nitric oxid

164 Our findings suggest that P2 receptors on group IV afferents play a role in evokin

165 ted by adenosine triphosphate acting through P2 receptors on SCs and intracellular signaling pathways

166 cellular purine degrading enzymes and P1 and P2 receptors on T cells isolated from the injured heart

167 hough animal studies suggest that purinergic P2 receptors on thin fibre sensory nerves are stimulated

168 ATP, by activating purinergic 2 (P2) receptors on group III and IV afferents, is thought

169 Gene-targeted mice for P1, P2 receptors, or ectonucleotidase exhibit only very mild

170 Apyrase, inhibition of P2 receptors, or inhibition of p38 MAPK with SB203580 re

171 demonstrate that the specific convergence of P2 receptor OSN axons is completely distorted in the FAF

172 Because plasma membrane-bound P2 receptors (P2R) mediate the effects of extracellular

173 hate (ATP) in the liver activates purinergic P2 receptors (P2R), which regulate inflammatory response

174 ected by extracellular nucleotides acting on P2 receptors (P2R); however, there remain uncertainties

175 (n)N', exert their physiological effects via P2 receptors (P2Rs).

176 nucleotides are exerted via two families of P2 receptors, P2X and P2Y.

177 s express nucleotide-gated G protein-coupled P2 receptors (P2YRs) and cation-conducting channels (P2X

178 increase stability to hydrolysis, preserved P2 receptor potency.

179 and Akt, thereby indicating a major role for P2 receptor/protein kinase signaling in TSP-1 expression

180 These data demonstrate that P2 receptors regulate macrophage activation in response

181 Activation of P2 receptors resulted in activation of an NHE-independen

182 The ATP then bound to macrophage nucleotide P2 receptors, resulting in activation of the NALP3/IL-1b

183 receptors has been compromised by a lack of P2 receptor-selective antagonist molecules.

184 eferential activation of specific subsets of P2 receptors sensitive to ADP (e.g., P2Y(1), P2Y(3), P2Y

185 entrations on airway epithelial surfaces for P2 receptor signaling and reduces by 6-fold adenosine pr

186 nction coupling and extracellular purinergic P2 receptor signaling between MLO-Y4 cells in a connecte

187 test a recently proposed role for purinergic P2 receptor signaling in central respiratory chemorecept

188 es played by these isozymes in modulation of P2 receptor signaling remain unclear.

189 ty has the potential to influence nucleotide P2 receptor signaling within the vasculature.

190 pathway involving conductive release of ATP, P2 receptor stimulation, and opening of membrane Cl- cha

191 were both dependent on extracellular ATP and P2 receptor stimulation.

192 s and on explanted rat skin, where different P2 receptor subtype agonists and antagonists were applie

193 the P1 receptor subtypes A2a and A2b and the P2 receptor subtype P2Y2, but not for the P1 receptor su

194 g a role for gliotransmission and the sites, P2 receptor subtype, and signalling mechanisms via which

195 g the length of the gut and characterize the P2-receptor subtype mediating fEPSPs.

196 P2 receptor subtypes and their signaling mechanisms were

197 gnificant implications for studies involving P2 receptor subtypes in bone.

198 emonstrated expression of the ATP-responsive P2 receptor subtypes P2Y(1), P2Y(2), and P2X(7), as well

199 These studies indicate that different P2 receptor subtypes play distinct roles in the modulati

200 However, the known repertoire of P2 receptor subtypes responsible for the proinflammatory

201 2X(7) receptor antagonists against the other P2 receptor subtypes such as the P2Y(2), P2X(4), and P2X

202 However, the P2 receptor subtypes underlying the contractile effects

203 tion requires concomitant signaling from two P2 receptor subtypes, P2Y1 and P2T(AC), coupled to G(q)

204 m cells expressing connexin43 and/or various P2 receptor subtypes.

205 However, the identification of P2 receptors subtypes and their native ligands, and the

206 ncentrations s and by number and features of P2 receptors summed with that generated by IP(3) diffusi

207 and fluid secretion via binding to membrane P2 receptors, though the physiological stimuli involved

208 s in vitro or in vivo; thus, the identity of P2 receptors underlying the purinergic component of RTN

209 olysaccharide has been suggested to activate P2 receptors via nucleotide release, we tested whether I

210 The involvement of P2 receptors was underscored in experiments with HEK cel

211 ellular ATP was hydrolyzed by apyrase or ATP/P2 receptors were blocked, injury-induced ERK activation

212 enosine, and partly due to the activation of P2 receptors which trigger the release of endogenous ade

213 ane receptors comprising two classes, P1 and P2 receptors, which are activated by adenosine and extra

214 ar ATP depletion with apyrase or blockade of P2 receptors with suramin.

215 However, after blocking P2 receptors with the broad-spectrum antagonists PPADS (

216 ed the functional role of type 2 purinergic (P2) receptors within the caudal aspect of the commissura