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1 ndicating the mediatory role of a purinergic P2 receptor.
2 nstrated that keratinocytes express multiple P2 receptors.
3 these two cell populations express different P2 receptors.
4 functionalities known to enhance potency at P2 receptors.
5 as previously unreported agonist activity at P2 receptors.
6 orm a bisphosphate, which reduced potency at P2 receptors.
7 e on the phenylazo ring modulated potency at P2 receptors.
8 not stem from activation of volume-sensitive P2 receptors.
9 ith molecular species other than ATP-binding P2 receptors.
10 cellular ATP acts directly on bone cells via P2 receptors.
11 ecto-ATPase and by suramin, an antagonist of P2 receptors.
12 ening of Cl- channels through stimulation of P2 receptors.
13 olecule through the activation of purinergic P2 receptors.
14 ological activities by activating purinergic P2 receptors.
15 lar ATP by way of the activation of specific P2 receptors.
16 crovascular EC through actions on purinergic 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
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
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
33 aves were not affected by apyrase, or by the P2 receptor agonists suramin (150 mum) or PPADS (50 mum)
34 nd UTP, and we compared the effects of these P2 receptor agonists with those of growth factors and ot
35 ere we discuss how signalling events through P2 receptors alter the outcomes of inflammatory or infec
37 elling elicits ATP release, which stimulates P2 receptors and activates Cl(-) channels, and that this
39 hibitory effects of antagonists of mammalian P2 receptors and calcium influx inhibitors on nucleotide
41 des increase proliferation via activation of P2 receptors and induction of calcium transients, while
42 ighly selective (IC50 >10 microM) over other P2 receptors and other neurotransmitter receptors, ion c
43 toma cells transfected to express individual P2 receptors and/or the gap junction protein connexin43.
44 i) ATP efflux, (ii) autocrine stimulation of P2 receptors, and (iii) increases in anion permeability
45 ists at the family of receptors known as the P2 receptors, and in keratinocytes the P2Y2 subtype is k
46 intracellular Ca(2+) concentration, whereas P2 receptor antagonism blocked DOR stimulation of inosit
47 nical strain and was completely blocked by a P2 receptor antagonist and by inhibition of p38/mitogen-
50 ATP receptors in the VLM (microinjection of P2 receptor antagonist pyridoxal-5'-phosphate-6-azopheny
51 and hP2X(2b) receptors were sensitive to the P2 receptor antagonist pyridoxal-5-phosphate-6-azophenyl
52 agal neurons which were blocked by the broad P2 receptor antagonist pyridoxal-phosphate-6-azophenyl-2
53 agal neurons which were blocked by the broad P2 receptor antagonist pyridoxal-phosphate-6-azophenyl-2
54 lphabetam-ATP were blocked completely by the P2 receptor antagonist pyridoxalphosphate-6-azophenyl-2'
60 ntagonist oxidized ATP (oATP) but not by the P2 receptor antagonist suramin; both ATP and BzATP incre
62 gent of ADP degradation), suramin (a general P2 receptor antagonist), pyridoxal 5'-phosphonucleotide
65 sly we have shown that injection of PPADS, a P2 receptor antagonist, into the arterial supply of skel
66 sion of GFAP and MMP-9 and a purinergic ATP (P2) receptor antagonist reduction in calcium response id
68 ist sulfonylphenyl theophylline, but not the P2-receptor antagonist suramin, antagonized the effect o
70 terms of insensitivity to blockade by known P2 receptor antagonists and the ineffectiveness of adeno
75 L67156 and were depressed in the presence of P2 receptor antagonists PPADS (10 microm) and suramin (5
77 s blocked by ionophoretic application of the P2 receptor antagonists suramin (0.02 M) and pyridoxal-p
82 ve antagonist, MRS2179, and the nonselective P2 receptor antagonists, pyridoxal phosphate 6-azophenyl
83 ed by apyrase inactivation of nucleotidases, P2 receptor antagonists, tetrodotoxin (TTX), or piroxica
93 hat ATP release and activation of purinergic P2 receptors are involved in melittin-induced ADAM activ
94 bilization and support the idea that several P2 receptors are involved in the regulation of different
97 es of respiratory neurone and the effects of P2 receptor blockade on CO2-evoked changes in activity i
99 y focal ATP application; however, purinergic P2-receptor blockade did not affect their CO2/H(+) respo
102 ificantly less sensitive to the nonselective P2 receptor blocker suramin than the UTP-mediated increa
103 hate-6-azophenyl-2',4'-disulfonate (PPADS, a P2 receptor blocker) decreased the ventilatory response
105 espiratory activity; however, injection of a P2-receptor blocker into this region had no effect on ba
106 -patch recordings from RTN neurons show that P2 receptor blockers decreased responsiveness to both 10
107 e apyrase (3 units/ml) or by exposure to the P2 receptor blockers suramin and Reactive Blue 2 (10-100
108 s much data to suggest roles for presynaptic P2 receptors but little to demonstrate which specific re
109 inflammation by acting on type 2 purinergic (P2) receptors, but the role of CD39 and CD39(+) Tregs in
111 singly recognized that stimulation of apical P2 receptors can influence solute transport in the nephr
115 through the interaction of nucleotides with P2 receptors, controls multiple biological responses.
116 xtracellular nucleotides, signalling through P2 receptors, could play an important role in modulating
117 ase and autocrine stimulation of purinergic (P2) receptors couple increases in cell volume to opening
120 Cs showed ATP unresponsiveness (secondary to P2-receptor desensitization) and impaired antigen-presen
125 fore hypothesized that activation of cardiac P2 receptor evokes CSR responses by stimulating cardiac
126 xternal stimuli, ionotropic and metabotropic P2 receptors, exo- and ecto-nucleotidases, second messen
128 s physiological responses through purinergic P2 receptors expressed in the plasma membrane of virtual
129 ut significant differences in the pattern of P2 receptor expression in mice and humans confer the div
133 ceptors, filling a long-standing need in the P2 receptor field, and are also important lead compounds
135 is and pharmacological profile of purinergic P2 receptors for extracellular nucleotides suggest that
136 ils are known to express several subtypes of P2 receptors for extracellular nucleotides, their functi
137 nities for specifically targeting individual P2 receptors for the treatment of inflammatory or infect
139 block Ca2+ entry induced by occupancy of the P2 receptor in two prostate cancer cell lines and inhibi
140 ferentially activates P2Y2 relative to other P2 receptors in MDCK-D1 cells (P2Y1 and P2Y11, as shown
141 Here, we report that ATP acts on purinergic P2 receptors in MNNs to potentiate in a Ca(2+) -dependen
142 There is also evidence that ATP may activate P2 receptors in preglomerular vessels, which may contrib
146 ruli that receive input from ORNs expressing P2 receptors in the P2-internal ribosome entry site-tau-
147 he effect of antagonizing, or desensitizing, P2 receptors in the retrofacial area of the ventrolatera
149 TP; scavenging endogenous ATP and inhibiting P2 receptors, in the absence of other stimuli, rapidly i
151 h kinetics revealed downregulation of select P2 receptors, including P2Y2R, in slow-growing hCPCs com
153 ked EMT, whereas treatment with a purinergic P2-receptor inhibitor or addition of apyrase demonstrate
157 in human astrocytes, and that signaling via P2 receptors may fine-tune the transcription of genes in
158 Therefore, aberrant regulation of nucleotide P2 receptors may influence angiogenesis in cd39-null mic
159 leotides, such as ATP and UTP, signaling via P2 receptors may provide a mechanism whereby cells can s
161 that in primary human fetal astrocytes, the P2 receptor-mediated and gap junction-mediated pathways
162 (50 microg/kg per min), to avoid endothelial P2 receptor-mediated effects on nitric oxide release cau
163 ulates cardiac sympathetic afferents through P2 receptor-mediated mechanism, and that opioid peptides
164 rsely, transmission of calcium waves via the P2 receptor-mediated pathway was potentiated in IL-1beta
165 ction-mediated pathway and an extracellular, P2 receptor-mediated pathway, which link the cells into
167 lease waves, local ejection of ATP triggered P2 receptor-mediated waves that were refractory to repea
171 low (via shear stress) or hypoxia, to act on P2 receptors on endothelial cells to produce nitric oxid
173 ted by adenosine triphosphate acting through P2 receptors on SCs and intracellular signaling pathways
174 cellular purine degrading enzymes and P1 and P2 receptors on T cells isolated from the injured heart
175 hough animal studies suggest that purinergic P2 receptors on thin fibre sensory nerves are stimulated
179 demonstrate that the specific convergence of P2 receptor OSN axons is completely distorted in the FAF
181 hate (ATP) in the liver activates purinergic P2 receptors (P2R), which regulate inflammatory response
182 ected by extracellular nucleotides acting on P2 receptors (P2R); however, there remain uncertainties
185 s express nucleotide-gated G protein-coupled P2 receptors (P2YRs) and cation-conducting channels (P2X
188 and Akt, thereby indicating a major role for P2 receptor/protein kinase signaling in TSP-1 expression
191 The ATP then bound to macrophage nucleotide P2 receptors, resulting in activation of the NALP3/IL-1b
193 eferential activation of specific subsets of P2 receptors sensitive to ADP (e.g., P2Y(1), P2Y(3), P2Y
194 entrations on airway epithelial surfaces for P2 receptor signaling and reduces by 6-fold adenosine pr
195 nction coupling and extracellular purinergic P2 receptor signaling between MLO-Y4 cells in a connecte
196 test a recently proposed role for purinergic P2 receptor signaling in central respiratory chemorecept
199 pathway involving conductive release of ATP, P2 receptor stimulation, and opening of membrane Cl- cha
201 s and on explanted rat skin, where different P2 receptor subtype agonists and antagonists were applie
202 the P1 receptor subtypes A2a and A2b and the P2 receptor subtype P2Y2, but not for the P1 receptor su
203 g a role for gliotransmission and the sites, P2 receptor subtype, and signalling mechanisms via which
207 emonstrated expression of the ATP-responsive P2 receptor subtypes P2Y(1), P2Y(2), and P2X(7), as well
210 2X(7) receptor antagonists against the other P2 receptor subtypes such as the P2Y(2), P2X(4), and P2X
212 tion requires concomitant signaling from two P2 receptor subtypes, P2Y1 and P2T(AC), coupled to G(q)
215 ncentrations s and by number and features of P2 receptors summed with that generated by IP(3) diffusi
216 and fluid secretion via binding to membrane P2 receptors, though the physiological stimuli involved
217 s in vitro or in vivo; thus, the identity of P2 receptors underlying the purinergic component of RTN
218 olysaccharide has been suggested to activate P2 receptors via nucleotide release, we tested whether I
220 ellular ATP was hydrolyzed by apyrase or ATP/P2 receptors were blocked, injury-induced ERK activation
221 enosine, and partly due to the activation of P2 receptors which trigger the release of endogenous ade
222 ane receptors comprising two classes, P1 and P2 receptors, which are activated by adenosine and extra
225 ed the functional role of type 2 purinergic (P2) receptors within the caudal aspect of the commissura