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1 h-promoting agent (acting at P2Y1, P2Y2, and P2X7 receptors).
2 al role in the transcriptional regulation of P2X7 receptor.
3 hought to be characteristic hallmarks of the P2X7 receptor.
4 o cellular responses typically attributed to P2X7 receptor.
5 S) stimulation and ATP signaling through the P2X7 receptor.
6 to be driven by unimpeded activation of the P2X7 receptor.
7 K(+) caused by stimulation of the purinergic P2X7 receptor.
8 a was unimpaired in macrophages deficient in P2X7 receptor.
9 of the extracellular loop of the full-length P2X7 receptor.
10 hly sensitive to that stimulated through the P2X7 receptor.
11 ing of a large pore at the recombinant human P2X7 receptor.
12 ess marked than for cells expressing the rat P2X7 receptor.
13 reatment for epilepsy based on targeting the P2X7 receptor.
14 ophages but not from macrophages lacking the P2X7 receptor.
15 esponse to SCI by activation of low-affinity P2X7 receptors.
16 l lines expressing recombinant human and rat P2X7 receptors.
17 ue-G, and KN-62, demonstrating activation of P2X7 receptors.
18 iate between the two widely used agonists at P2X7 receptors.
19 inhibitor Z-VADfmk, and requires functional P2X7 receptors.
20 with DNA fragmentation, and does not require P2X7 receptors.
21 ifferentially regulated by the activation of P2X7 receptors.
22 stably express the human or rat recombinant P2X7 receptors.
23 a(2+) permeability are difficult to apply to P2X7 receptors.
24 asses that selectively target P2X1, P2X3, or P2X7 receptors.
25 human embryonic kidney cells expressing rat P2X7 receptors.
26 nergistically up-regulated mRNA encoding the P2X7 receptor, a recently cloned ATP-gated channel that
27 mma disrupts the functionality of purinergic P2X7 receptors, a key step controlling eCB production by
29 e investigated whether LTB4 is produced upon P2X7 receptor activation and examined whether LTB4 modul
33 investigated for dependence upon caspase-1, P2X7 receptor activation, and loss of membrane asymmetry
37 astrocytes with properties characteristic of P2X7 receptor activation: the current was amplified in l
39 ll patch clamp studies, exposure to the P2X4/P2X7 receptor agonist 2'3'-O-(4-benzoyl-benzoyl)-adenosi
44 ed treatment with lipopolysaccharide and the P2X7 receptor agonist, benzylated ATP, suggesting that n
45 ess functional purinergic receptors and that P2X7 receptor agonists significantly reduce cell numbers
47 n the plasma membrane, but activation of the P2X7 receptor also leads to rapid cytoskeletal re-arrang
48 to be partially mediated by activation of a P2X7 receptor, although hybrid channels cannot be ruled
49 P2Y2, P2Y4, P2Y6, and P2Y12, and at P2X4 and P2X7 receptors), an immunosuppressant (acting at P2Y11),
50 ng mechanisms were prevented by knocking out P2X7 receptor and by the use of specific antagonists.
55 n experiments with HEK cells, which lack the P2X7 receptor and showed strikingly increased response t
56 S. aureus supernatant was independent of the P2X7 receptor and the essential TLR adaptors MyD88 and T
57 ess a low activation threshold allele of the P2X7 receptor and the P2X7 gene maps to a locus associat
58 derived macrophage cells natively expressing P2X7 receptors and cells transfected with human P2X7 but
61 g lipin-2 decreases ion currents through the P2X7 receptor, and downstream events that drive IL-1beta
63 he centrally available, potent, and specific P2X7 receptor antagonist JNJ-47965567 (30 mg/kg) signifi
65 f both cytokines was blocked completely by a P2X7 receptor antagonist, oxidized ATP, and partially by
66 reatment of RAW 264.7 macrophages with a P2Z/P2X7 receptor antagonist, periodate oxidized adenosine 5
73 ular constituent immunoreactive for specific P2X7 receptor antiserum in the kainate-induced seizure a
77 pressing a rat P2X7 receptor indicating that P2X7 receptors are not involved in stimulation of ATP re
80 pore-forming properties of human and rodent P2X7 receptors are sensitive to perturbations of cholest
81 ive stress in ALS microglia and identify the P2X7 receptor as a promising target for the development
85 f pannexin-1-hemichannel (PNX1) coupled with P2X7-receptor blocks the infection-induced eATP release
86 of fluorescent dyes in many cells expressing P2X7 receptors, but controversy persists as to whether s
87 , in SOD1-G93A microglia, the stimulation of P2X7 receptor by 2'-3'-O-(benzoyl-benzoyl) ATP enhanced
88 onic kidney cells that interact with the rat P2X7 receptor, by affinity purification followed by mass
89 lts demonstrate that the open channel of the P2X7 receptor can allow passage of molecules with sizes
90 itionally, it has been demonstrated that the P2X7 receptor can induce PLA2 activation and arachidonic
91 , we evaluated whether antagonism of the P2Z/P2X7 receptor can influence LPS signaling and expression
94 de during activation by endogenous ATP-gated P2X7 receptor channels, the exogenous bacterial ionophor
96 we present crystal structures of a mammalian P2X7 receptor complexed with five structurally-unrelated
97 Considering that extracellular ATP through P2X7 receptor constitutes a neuron-to-microglia alarm si
98 rs controlling proliferation, while P2X5 and P2X7 receptors control early differentiation, terminal d
101 eptic mice displayed enhanced agonist-evoked P2X7 receptor currents, and synaptosomes from these anim
103 fficient to induce motor neuron death by the P2X7 receptor-dependent activation of the Fas pathway.
106 The generation of prothrombotic MPs required P2X7 receptor-dependent production of ROS leading to inc
107 e data suggest that PDI regulates a critical P2X7 receptor-dependent signaling pathway that generates
108 c receptor P2X, ligand-gated ion channel, 7 (P2X7 receptor; encoded by P2rx7) induced activation (dec
109 These results were relevant in vivo since P2X7 receptor expression was upregulated in a P. gingiva
110 tative measures of the Ca(2+) current of the P2X7 receptor for the first time, and suggest that the c
112 study, we investigate the effect of loss of P2X7 receptor function on retinal structure and function
118 he present study suggests that targeting the P2X7 receptor has anticonvulsant and possibly disease-mo
120 lly relevant strategy by which to antagonize P2X7 receptors has yet, to the best of our knowledge, be
121 ular ATP signaling, particularly through the P2X7 receptor, has considerable translational potential,
122 sue, followed by activation of high-affinity P2X7 receptors, has previously been implicated in second
123 idely distributed in the nervous system, and P2X7 receptors have roles in neuropathic pain and in the
124 normal mice or those in which genes for the P2X7 receptor, IL-1beta, IL-1alpha, IL-18, or caspase-1
125 pothesized that the ATP-activated macrophage P2X7 receptors implicated in nucleotide-mediated macroph
128 ent study shows that loss of function of the P2X7 receptor in mice induces retinal changes representi
132 study demonstrated functional expression of P2X7 receptors in non-neuronal but not in small diameter
133 In the present study, the expression of P2X7 receptors in non-neuronal cells and neurons isolate
134 showed that prolonged agonist activation of P2X7 receptors in non-neuronal cells did not lead to cyt
136 In addition, the released ATP activates P2X7 receptors in satellite cells that enwrap each DRG n
139 ophages; however, only monocytes also showed P2X7 receptor-independent release of mature IL-1beta.
140 K293 cells and HEK293 cells expressing a rat P2X7 receptor indicating that P2X7 receptors are not inv
141 In addition, the sustained activation of P2X7 receptors inhibited cell-to-cell electrotonic trans
142 le translational potential, given that novel P2X7-receptor inhibitors are already available for clini
149 well as wild-type mice, suggesting that the P2X7 receptor is not required for control of pulmonary M
151 In our study, we show that the ATP-gated P2X7 receptor is upregulated in experimental epilepsy an
152 unctional studies, our data suggest that the P2X7 receptor itself constitutes a lipid-composition dep
153 xogenous LTB4, and macrophages obtained from P2X7 receptor knockout mice eliminated L. amazonensis wh
154 tochemical studies on human lymphoid tissue, P2X7 receptor labeling was observed within discrete area
155 at hyperoxia induces K(+) efflux through the P2X7 receptor, leading to inflammasome activation and se
156 indings suggest a noxious mechanism by which P2X7 receptor leads to enhanced oxidative stress in ALS
158 ptosomes from these animals showed increased P2X7 receptor levels and altered calcium responses.
159 tivation by mithramycin A reduced endogenous P2X7 receptor levels in primary cultures of cortical neu
161 Gln have >85% loss of 'pore' function of the P2X7 receptor measured by ATP-induced ethidium uptake.
163 infection inhibits extracellular-ATP (eATP)/P2X7-receptor mediated cell death in gingival epithelial
164 lagellin proceeds normally in the absence of P2X7 receptor-mediated cytoplasmic K(+) perturbations.
167 In summary, these data suggest that the P2Z/P2X7 receptor modulates LPS-induced macrophage activatio
168 one (compound 35), were found to have robust P2X7 receptor occupancy at low doses in rat with ED50 va
170 the agonist-gated Ca(2+) flux of recombinant P2X7 receptors of dog, guinea pig, human, monkey, mouse,
171 3cr1-deficient MPs express increased surface P2X7 receptor (P2RX7), which stimulates IL-1beta maturat
176 the pore of the monovalent cation-selective P2X7 receptor (P2X7R) expands to accommodate large molec
177 Here, we demonstrate that stimulation of the P2X7 receptor (P2X7R) for ATP alkalinizes lysosomes in c
179 nine (Arg, R) at codon 460 of the purinergic P2X7 receptor (P2X7R) has repeatedly been associated wit
188 previously that activation of the purinergic P2X7 receptor (P2X7R) triggers sAPPalpha shedding from n
189 ctive pores similar to those elicited by the P2X7 receptor (P2X7R), an ATP-gated cation channel expre
191 ling purinergic receptors, predominantly the P2X7 receptor (P2X7R), via an ATP analog initiate innate
194 enin release (>/=2-fold), whereas purinergic P2X7 receptors (P2X7R) blockade with A740003 (3 microM)
197 gh the inhibition of the P2X purinoceptor 7 (P2X7) receptor (P2X7R), an ATP-gated ion channel, and a
202 o ethidium (Etd(+)) and Ca(2+) by activating P2X7 receptors (P2X7Rs) that open pannexin hemichannels
203 tracellular ATP binds to and signals through P2X7 receptors (P2X7Rs) to modulate immune function in b
204 we found that infection with H37Ra inhibits P2X7 receptor (P2XR) signals and that CsA restores P2XR
207 sion of the death signal requires functional P2X7 receptors, pointing to a role for these receptors i
208 eveal cholesterol as a negative regulator of P2X7 receptor pore formation, protecting cells from P2X7
209 MoAb was used to immunoprecipitate the human P2X7 receptor protein, and in immunohistochemical studie
213 -1 hemichannels to the immune synapse, while P2X7 receptors remain uniformly distributed on the cell
217 tly, we identified a novel pathway involving P2X7 receptor scavenger function expressed on ocular imm
218 Whole-cell recordings from cells expressing P2X7 receptors showed that this markedly reduced subsequ
227 lar amounts of ATP, activation of purinergic P2X7 receptors, sustained rise in intracellular calcium,
228 uncovered a novel site (Y382-384) within the P2X7 receptor that can be targeted to blunt the developm
229 drial ATP production, and stimulate P2X4 and P2X7 receptors that elicit interleukin 2 production and
232 iggers, through activation of the purinergic P2X7 receptor, the formation of the inflammasome, a mult
233 om a human monocyte library that encodes the P2X7 receptor; the predicted protein is 80% identical to
234 m channels is less potent than inhibition of P2X7 receptors, there may be significant inhibition of s
236 ctivates the inflammasome via the purinergic P2X7 receptor to cause inflammation and hyperoxic acute
238 ns circumvent the requirement of ATP and the P2X7 receptor to induce caspase-1 activation via Nlrp3.
239 OD1-G93A mice and SOD1-G93A mice lacking the P2X7 receptor to investigate the effects of both pharmac
241 cells, the activation of M3AChRs stimulates P2X7 receptors to increase [Ca2+]i and protein secretion
242 ing pathways that overlap with those used by P2X7 receptors to increase [Ca2+]i, but they also use si
243 to become self sustaining through action of P2X7 receptors to open pannexin hemichannels and then co
245 ed SAPK activation could be recapitulated in P2X7 receptor-transfected HEK293 cells, but not in wild-
246 strate that ATP signaling through macrophage P2X7 receptors uncouples the thioredoxin (TRX)/TRX reduc
251 blue G (BBG), best known as an antagonist of P2X7 receptors, was found to inhibit voltage-gated sodiu
255 ly as the channel opened, in contrast to the P2X7 receptor where the NMDG permeability develops over
256 vation of macrophage surface-associated P2Z (P2X7) receptors, which are one of the purinergic recepto
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