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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
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 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
36                   However, the roles of both P2 receptor and endogenous opioids in cardiac sympathoex
37 elling elicits ATP release, which stimulates P2 receptors and activates Cl(-) channels, and that this
38                          We hypothesize that P2 receptors and adenosine transporters could be novel t
39 hibitory effects of antagonists of mammalian P2 receptors and calcium influx inhibitors on nucleotide
40 ed via nucleotides (ATP, UTP) binding apical P2 receptors and increasing [Ca(2+)](i).
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-
48          Attenuation of this response by the P2 receptor antagonist PPADS suggests that bradykinin-in
49                       Novel analogues of the P2 receptor antagonist pyridoxal-5'-phosphate 6-azopheny
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'
55                                              P2 receptor antagonist studies indicated a role for P2X2
56                    These were blocked by the P2 receptor antagonist suramin (100 microm).
57                                          The P2 receptor antagonist suramin decreased liver injury in
58                                          The P2 receptor antagonist suramin inhibited these intercell
59 lement pathway Ab eculizumab, the purinergic P2 receptor antagonist suramin, and EDTA.
60 ntagonist oxidized ATP (oATP) but not by the P2 receptor antagonist suramin; both ATP and BzATP incre
61             In the isolated retina, suramin (P2 receptor antagonist) reduces the frequency of spontan
62 gent of ADP degradation), suramin (a general P2 receptor antagonist), pyridoxal 5'-phosphonucleotide
63                      Suramin, a nonselective P2 receptor antagonist, and MRS-2179, a P2Y1 receptor-se
64          Suramin (500 mum), a broad-spectrum P2 receptor antagonist, dilated retinal arterioles by 50
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
67                       In the presence of the P2-receptor antagonist suramin (0.1 mM), the amplitude o
68 ist sulfonylphenyl theophylline, but not the P2-receptor antagonist suramin, antagonized the effect o
69                           In the presence of P2 receptor antagonists A2P5P or AR-C67085, LIBS6 failed
70  terms of insensitivity to blockade by known P2 receptor antagonists and the ineffectiveness of adeno
71                      However, treatment with P2 receptor antagonists did not alter the ratio of nesti
72 n, and the acyclic approach to the design of P2 receptor antagonists is valid.
73                                              P2 receptor antagonists or P2Y(6) antisense oligonucleot
74                                   Similarly, P2 receptor antagonists or SC49992 blocked ADP-induced a
75 L67156 and were depressed in the presence of P2 receptor antagonists PPADS (10 microm) and suramin (5
76                             Analogues of the P2 receptor antagonists pyridoxal-5'-phosphate and the 6
77 s blocked by ionophoretic application of the P2 receptor antagonists suramin (0.02 M) and pyridoxal-p
78 0.1-30 micrometer) and were sensitive to the P2 receptor antagonists suramin and iso-PPADS.
79                                          The P2 receptor antagonists suramin and pyridoxalphosphate-6
80            These effects were blocked by the P2 receptor antagonists XAMR 0721, periodate-oxidized AT
81              Pretreatment of astrocytes with P2 receptor antagonists, including suramin and periodate
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
84 n the absence of factor B, and by purinergic P2 receptor antagonists.
85 reduced or abolished by prior application of P2 receptor antagonists.
86 (2+)]i oscillations, which were abolished by P2 receptor antagonists.
87 dently reduced in the presence of ATPases or P2 receptor antagonists.
88 l CO2/H+ sensitivity by an amount similar to P2 receptor antagonists.
89 ng expansion, and were reversibly blocked by P2 receptor antagonists.
90                                Activation of P2 receptors appears to influence endothelial cell chemo
91                                              P2 receptors are expressed during muscle development, an
92                                        Since P2 receptors are generally coupled to Ca(2+) signaling p
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
95           Nucleotides, acting as agonists at P2 receptors, are important extracellular signaling mole
96                           Type 2 purinergic (P2) receptors bind extracellular nucleotides and are exp
97 es of respiratory neurone and the effects of P2 receptor blockade on CO2-evoked changes in activity i
98 P, the CO2-evoked effects were unaffected by P2 receptor blockade.
99 y focal ATP application; however, purinergic P2-receptor blockade did not affect their CO2/H(+) respo
100 tive raphe neurons were unaffected by ATP or P2-receptor blockade.
101          These effects were abolished by the P2 receptor blocker suramin (0.02 M, 80 nA), which also
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
104                       Injections of ATP or a P2-receptor blocker into the medullary raphe had no effe
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
110                   Activation of a purinergic P2 receptor by adenosine 5'-triphosphate (ATP) has previ
111 singly recognized that stimulation of apical P2 receptors can influence solute transport in the nephr
112 ophs, and that these actions are mediated by P2 receptor channels.
113 we could assess the indomethacin-insensitive P2 receptor component.
114                      These data suggest that P2 receptors contribute to the exercise pressor reflex i
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
118 s, thereby modulating the type-2 purinergic (P2) receptors demonstrated on these cells.
119  increased breathing and blood pressure by a P2-receptor-dependent mechanism.
120 Cs showed ATP unresponsiveness (secondary to P2-receptor desensitization) and impaired antigen-presen
121 ative and provide a potential new avenue for P2 receptor drug development.
122                              We have applied P2 receptor drugs to rat pial arterioles and measured ch
123                                  Blockage of P2 receptors eliminated the effect of ATP on the OHC ele
124 tors in the microenvironment, and pattern of P2 receptor engagement.
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
127                   The effect of these PGs on P2 receptors expressed in murine and human macrophages w
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
130                         Here, we investigate P2 receptor expression in primary human monocyte-derived
131 , with a selectivity for that subtype of the P2 receptor family of >1000-fold.
132 itions and act as ligands for members of the P2 receptor family.
133 ceptors, filling a long-standing need in the P2 receptor field, and are also important lead compounds
134  classified as P1 receptors for adenosine or P2 receptors for ATP.
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
138                      Signaling by purinergic P2 receptors has previously been linked to the antimycob
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
143                  Consistent with the role of P2 receptors in signaling and secretion, the actions of
144                                  The role of P2 receptors in synaptic transmission to the rat medial
145  their regulation by basolateral and luminal P2 receptors in the duct.
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
148  processes through activation of nucleotide (P2) receptors in the plasma membrane.
149 TP; scavenging endogenous ATP and inhibiting P2 receptors, in the absence of other stimuli, rapidly i
150                                          The P2 receptors, including P2X and P2Y purinoceptor subtype
151 h kinetics revealed downregulation of select P2 receptors, including P2Y2R, in slow-growing hCPCs com
152 he soluble ecto-nucleotidase apyrase and the P2 receptor inhibitor suramin.
153 ked EMT, whereas treatment with a purinergic P2-receptor inhibitor or addition of apyrase demonstrate
154                                              P2 receptor inhibitors, including oxidized ATP, blocked
155                     Nucleotide activation of P2 receptors is important in autocrine and paracrine reg
156                                Inhibition of P2 receptors limited oxidative stress-induced senescence
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
160                                     Although P2 receptors mediate a myriad of physiological effects o
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
166            From these data, we conclude that P2 receptor-mediated signaling intersects with that of I
167 lease waves, local ejection of ATP triggered P2 receptor-mediated waves that were refractory to repea
168        Nucleotides exert these functions via P2-receptor-mediated mechanisms that can also interact w
169       Adenosine triphosphate (ATP) acting at P2 receptors mediates some fast excitatory postsynaptic
170                                          The P2 receptor mediating the antiapoptotic actions of ATP w
171 low (via shear stress) or hypoxia, to act on P2 receptors on endothelial cells to produce nitric oxid
172                    Our findings suggest that P2 receptors on group IV afferents play a role in evokin
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
176             ATP, by activating purinergic 2 (P2) receptors on group III and IV afferents, is thought
177                   Gene-targeted mice for P1, P2 receptors, or ectonucleotidase exhibit only very mild
178                       Apyrase, inhibition of P2 receptors, or inhibition of p38 MAPK with SB203580 re
179 demonstrate that the specific convergence of P2 receptor OSN axons is completely distorted in the FAF
180                Because plasma membrane-bound P2 receptors (P2R) mediate the effects of extracellular
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
183 (n)N', exert their physiological effects via P2 receptors (P2Rs).
184  nucleotides are exerted via two families of P2 receptors, P2X and P2Y.
185 s express nucleotide-gated G protein-coupled P2 receptors (P2YRs) and cation-conducting channels (P2X
186                                              P2 receptors play critical roles in a variety of animal
187  increase stability to hydrolysis, preserved P2 receptor potency.
188 and Akt, thereby indicating a major role for P2 receptor/protein kinase signaling in TSP-1 expression
189                  These data demonstrate that P2 receptors regulate macrophage activation in response
190                                Activation of P2 receptors resulted in activation of an NHE-independen
191  The ATP then bound to macrophage nucleotide P2 receptors, resulting in activation of the NALP3/IL-1b
192  receptors has been compromised by a lack of P2 receptor-selective antagonist molecules.
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
197 es played by these isozymes in modulation of P2 receptor signaling remain unclear.
198 ty has the potential to influence nucleotide P2 receptor signaling within the vasculature.
199 pathway involving conductive release of ATP, P2 receptor stimulation, and opening of membrane Cl- cha
200 were both dependent on extracellular ATP and P2 receptor stimulation.
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
204 g the length of the gut and characterize the P2-receptor subtype mediating fEPSPs.
205                                              P2 receptor subtypes and their signaling mechanisms were
206 gnificant implications for studies involving P2 receptor subtypes in bone.
207 emonstrated expression of the ATP-responsive P2 receptor subtypes P2Y(1), P2Y(2), and P2X(7), as well
208        These studies indicate that different P2 receptor subtypes play distinct roles in the modulati
209             However, the known repertoire of P2 receptor subtypes responsible for the proinflammatory
210 2X(7) receptor antagonists against the other P2 receptor subtypes such as the P2Y(2), P2X(4), and P2X
211                                 However, the P2 receptor subtypes underlying the contractile effects
212 tion requires concomitant signaling from two P2 receptor subtypes, P2Y1 and P2T(AC), coupled to G(q)
213 m cells expressing connexin43 and/or various P2 receptor subtypes.
214               However, the identification of P2 receptors subtypes and their native ligands, and the
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
219                           The involvement of P2 receptors was underscored in experiments with HEK cel
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
223 ar ATP depletion with apyrase or blockade of P2 receptors with suramin.
224                      However, after blocking P2 receptors with the broad-spectrum antagonists PPADS (
225 ed the functional role of type 2 purinergic (P2) receptors within the caudal aspect of the commissura

 
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