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1 in was potentiated by ADP acting through the P2Y12 receptor.
2 largely independent of signaling through the P2Y12 receptor.
3 lepsy or peritumoral cortex tissue expressed P2Y12 receptors.
4 ATP release, and microglial response through P2Y12 receptors.
5 d an autocrine ADP-mediated response through P2Y12 receptors.
6 onal activation and blocked by inhibition of P2Y12 receptors.
7  addition to that derived from antagonism of P2Y12 receptors.
8  CysLT1R and CysLT2R but not in mice lacking P2Y12 receptors.
9 y active, and its activity is potentiated by P2Y12 receptors.
10 d in the initiation of platelet aggregation, P2Y12 receptor activation appears to account for the bul
11 process outgrowth to damaged tissue requires P2Y12 receptor activation but is unaffected by blocking
12                    Furthermore, we show that P2Y12 receptor activation is not required for protease-a
13  of a local thrombus, dual inhibition of the P2Y12 receptor and calcium mobilization result in a comp
14 ivation markers including CD45, CD11b/c, and p2y12 receptor and evaluated their activation state usin
15 is dependent on both the G(alpha)(i)-coupled P2Y12 receptor and the G(alpha)(q)-coupled P2Y1 receptor
16 mole inhibit platelet function by inhibiting P2Y12 receptors and platelet phosphodiesterase, respecti
17 lular traps had little effects, but platelet P2Y12 receptor antagonism with clopidogrel, fibrinolysis
18  supporting pleiotropic effects coupled with P2Y12 receptor antagonism.
19 s a potent, highly selective, and reversible P2Y12 receptor antagonist and by far the most potent inh
20 ubstituents on the ribose and base conferred P2Y12 receptor antagonist properties to these molecules
21                   The direct-acting platelet P2Y12 receptor antagonist ticagrelor can reduce the inci
22                                          The P2Y12 receptor antagonist ticagrelor has been shown to b
23 escribed an additional mode of action of the P2Y12 receptor antagonist ticagrelor.
24              On the other hand, apyrase, the P2Y12 receptor antagonist, AR-C67085, and indomethacin o
25      However, pretreatment of platelets with P2Y12 receptor antagonist, AR-C69331MX did not interfere
26 on of platelets with aspirin, but not with a P2Y12 receptor antagonist, caused a marked reduction in
27 d by either the integrin inhibitor RGDS or a P2Y12 receptor antagonist, indicating a requirement for
28       Physicians considering prescription of P2Y12-receptor antagonist for long-term (>1 year) protec
29 heral arterial disease, or following a brief P2Y12-receptor antagonist interruption, whereas clopidog
30  Platelet inhibitory effects induced by oral P2Y12 receptor antagonists are delayed in patients with
31 lar patients who smoke benefit from platelet P2Y12 receptor antagonists more than their nonsmoking pe
32 ntagonists), cyclopentyltriazolopyrimidines (P2Y12 receptor antagonists), anti-von Willebrand factor
33 al study, consisting of the thienopyridines (P2Y12 receptor antagonists), cyclopentyltriazolopyrimidi
34 morphine and its potential interactions with P2Y12 receptor antagonists, as well as on the central is
35                                              P2Y12 receptor antagonists, concurrently administered wi
36                         It was suppressed by P2Y12 receptor antagonists, which also reduced process l
37 lial process extension, which was blocked by P2Y12 receptor antagonists.
38   As head-to-head comparative trials between P2Y12-receptor antagonists are lacking, selection of a s
39 r and inside-out signaling from the P2Y1 and P2Y12 receptors are necessary for phospholipase A(2) act
40                                     Platelet P2Y12 receptors are the targets of very widely used anti
41 namides, which are potent antagonists of the P2Y12 receptor, are presented.
42       The powerful antithrombotic effects of P2Y12 receptor blockers may, in part, be mediated by pro
43 P did not require Gi signaling or functional P2Y12 receptors but was mediated through activation of a
44                                Both P2Y1 and P2Y12 receptors can also undergo PMA-stimulated internal
45 eas pharmacological blockade of G(i)-coupled P2Y12 receptors decreased sleep.
46                          In platelets from a P2Y12 receptor-defective patient, alpha-thrombin, SFLLRN
47 duced changes at somatic junctions triggered P2Y12 receptor-dependent microglial neuroprotection, reg
48 rful synergism is explained by blockade of a P2Y12 receptor-dependent, NO/cGMP-insensitive phosphatid
49  epinephrine (alpha(2A)-adrenergic) and ADP (P2Y12) receptors display strong preferences among G(i) f
50  thus reduces surveillance, whereas blocking P2Y12 receptors does not affect membrane potential, rami
51       Here we show that blockade of platelet P2Y12 receptors dramatically enhances the antiplatelet p
52                                              P2Y12 receptor expression by LAD2 cells is required for
53                                              P2Y12 receptor expression permits LTE4-induced activatio
54 26 directly and indirectly affects ADAM9 and P2Y12 receptor expression.
55 ently identified functional effector for the P2Y12 receptor, in the regulation of ADP-induced TXA2 ge
56 treatment platelet reactivity and incomplete P2Y12 receptor inhibition are risk factors for SAT.
57 stenting and treatment strategies to improve P2Y12 receptor inhibition in patients with high post-tre
58 phoprotein phosphorylation levels to measure P2Y12 receptor inhibition were determined (n = 20) and c
59 pidogrel metabolism, potentially attenuating P2Y12 receptor inhibition.
60  with stenting, treatment with aspirin and a P2Y12 receptor inhibitor also becomes indicated.
61 studies, mice were treated with the platelet P2Y12 receptor inhibitor clopidogrel or placebo.
62 by single antiplatelet therapy (SAPT) with a P2Y12 receptor inhibitor confers benefits compared with
63 t therapy (DAPT) with aspirin and a platelet P2Y12 receptor inhibitor is the standard antithrombotic
64 Ticagrelor (Brilinta), a commonly prescribed P2Y12 receptor inhibitor used after myocardial infarctio
65 sk in major bleeding by combining aspirin, a P2Y12 receptor inhibitor, and an anticoagulant.
66 me (ACS) patients are not pre-treated with a P2Y12 receptor inhibitor, and percutaneous coronary inte
67 d to treat excessive bleeding in patients on P2Y12 receptor inhibitors (RI).
68                                              P2Y12 receptor inhibitors clinically in use such as clop
69  after discharge for beta-blockers, platelet P2Y12 receptor inhibitors, statins, and angiotensin-conv
70 ess and novel platelet adenosine diphosphate P2Y12 receptor inhibitors.
71 elor and prasugrel are guideline-recommended P2Y12 receptor inhibitors.
72 ilar to that of rodent microglia in that the P2Y12 receptor initiates process extension.
73                                     Blocking P2Y12 receptor is a clinically well-validated strategy f
74                                    Thus, the P2Y12 receptor is required for proinflammatory actions o
75 uated by PKC inhibitors, whereas that of the P2Y12 receptor is unaffected.
76 osine diphosphate (ADP)-reactive purinergic (P2Y12) receptor is required for LTE4-mediated pulmonary
77 Because clopidogrel antagonizes the platelet P2Y12 receptor, it is widely prescribed for patients wit
78                   Ligand docking on P2Y1 and P2Y12 receptor models was guided by mutagenesis results,
79           In platelets from mice lacking the P2Y12 receptor, neither alpha-thrombin nor AYPGKF caused
80 ntial signalling and cell activation through P2Y12 receptor or receptor heterodimers but no specific
81                               A platelet ADP P2Y12 receptor (P2Y12) inhibitor plus aspirin is standar
82                                    The human P2Y12 receptor (P2Y12-R) is a member of the G protein co
83                                              P2Y12 receptor (P2Y12-R) signaling is mediated through G
84     Ticagrelor is a potent antagonist of the P2Y12 receptor (P2Y12R) and consequently an inhibitor of
85 ed BSM contraction is blocked by a selective P2Y12 receptor (P2Y12R) antagonist, PSB 0739 (25 muM), b
86                      Defects of the platelet P2Y12 receptor (P2Y12R) for adenosine diphosphate (ADP)
87                                Recently, the P2Y12 receptor (P2Y12R) has been identified as a promisi
88 sence of microglia or blockade of microglial P2Y12 receptor (P2Y12R) substantially impairs neurovascu
89                                          The P2Y12 receptor (P2Y12R), one of eight members of the P2Y
90 th tests measuring the adenosine diphosphate-P2Y12 receptor pathway, without significant variations i
91                                     Platelet P2Y12 receptors play a central role in the regulation of
92 elated factors (higher on-treatment platelet P2Y12 receptor reactivity and premature thienopyridine d
93 ene adenosine 5'-triphosphate (AR-C67085), a P2Y12 receptor-selective antagonist, and adenosine-2'-ph
94  inhibited in the presence of AR-C69931MX, a P2Y12 receptor-selective antagonist, or GF 109203X, a pr
95 or that abolishes secretion, or AR-C66096, a P2Y12 receptor-selective antagonist; alpha-thrombin-indu
96                               Cloning of the P2Y12 receptor should facilitate the development of bett
97  PMA reduced subsequent ADP-induced P2Y1 and P2Y12 receptor signaling.
98 ators is ADP, which, acting through platelet P2Y12 receptors, strongly amplifies aggregation.
99                    We use CD45, CD11b/c, and p2y12 receptor to identify microglia and evaluate their
100 X1, and A2b receptors was unchanged, whereas P2Y12 receptor was significantly downregulated, suggesti
101 in undergoes synergy with ADP acting via the P2Y12 receptor whereas there is no synergy via the P2Y1

 
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