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1 in was potentiated by ADP acting through the P2Y12 receptor.
2 y active, and its activity is potentiated by P2Y12 receptors.
3 ATP release, and microglial response through P2Y12 receptors.
4 d an autocrine ADP-mediated response through P2Y12 receptors.
5 addition to that derived from antagonism of P2Y12 receptors.
6 CysLT1R and CysLT2R but not in mice lacking P2Y12 receptors.
7 ated by adenosine-5'-diphosphate through the P2Y(12) receptor.
8 receptor present on platelets, that is, the P2Y(12) receptor.
9 ing that they do not directly antagonize the P2Y(12) receptor.
10 of the functional responses of the platelet P2Y(12) receptor.
11 ically among these mutants and the wild-type P2Y(12) receptor.
12 h the extracellular cysteine residues on the P2Y(12) receptor.
13 ) to ADP, the specific agonist of P2Y(1) and P2Y(12) receptors.
14 ressing high levels of recombinant P2Y(2) or P2Y(12) receptors.
15 naling pathways linked to the P2X4, P2X7 and P2Y(12) receptors.
18 d in the initiation of platelet aggregation, P2Y12 receptor activation appears to account for the bul
19 process outgrowth to damaged tissue requires P2Y12 receptor activation but is unaffected by blocking
21 osine 5'-triphosphate), an antagonist of the P2Y(12) receptor, also did not differ dramatically among
22 rugs, clopidogrel and CS-747, inactivate the P2Y(12) receptor and are predicted to interact with the
24 nstitutively active mutant of human platelet P2Y(12) receptor and the identification of potent invers
25 of a local thrombus, dual inhibition of the P2Y12 receptor and calcium mobilization result in a comp
26 is dependent on both the G(alpha)(i)-coupled P2Y12 receptor and the G(alpha)(q)-coupled P2Y1 receptor
27 mole inhibit platelet function by inhibiting P2Y12 receptors and platelet phosphodiesterase, respecti
28 de bridges with both Cys17 and Cys270 in the P2Y(12) receptor, and thereby inactivate the receptor.
30 A protein kinase C inhibitor GF 109203X or a P2Y(12) receptor antagonist AR-C69931MX partly reduced G
33 47, LY640315), a novel potent thienopyridine P2Y(12) receptor antagonist, has the potential to achiev
35 s a potent, highly selective, and reversible P2Y12 receptor antagonist and by far the most potent inh
36 ubstituents on the ribose and base conferred P2Y12 receptor antagonist properties to these molecules
42 on of platelets with aspirin, but not with a P2Y12 receptor antagonist, caused a marked reduction in
43 d by either the integrin inhibitor RGDS or a P2Y12 receptor antagonist, indicating a requirement for
45 heral arterial disease, or following a brief P2Y12-receptor antagonist interruption, whereas clopidog
46 in platelet activation and is the target of P2Y(12) receptor antagonists that have proven therapeuti
47 Platelet inhibitory effects induced by oral P2Y12 receptor antagonists are delayed in patients with
48 lar patients who smoke benefit from platelet P2Y12 receptor antagonists more than their nonsmoking pe
49 ntagonists), cyclopentyltriazolopyrimidines (P2Y12 receptor antagonists), anti-von Willebrand factor
50 al study, consisting of the thienopyridines (P2Y12 receptor antagonists), cyclopentyltriazolopyrimidi
51 morphine and its potential interactions with P2Y12 receptor antagonists, as well as on the central is
53 As head-to-head comparative trials between P2Y12-receptor antagonists are lacking, selection of a s
54 r and inside-out signaling from the P2Y1 and P2Y12 receptors are necessary for phospholipase A(2) act
59 P did not require Gi signaling or functional P2Y12 receptors but was mediated through activation of a
60 the reactive cysteine residues on the human P2Y(12) receptor by site-directed mutagenesis using pCMB
63 rful synergism is explained by blockade of a P2Y12 receptor-dependent, NO/cGMP-insensitive phosphatid
65 epinephrine (alpha(2A)-adrenergic) and ADP (P2Y12) receptors display strong preferences among G(i) f
66 thus reduces surveillance, whereas blocking P2Y12 receptors does not affect membrane potential, rami
68 hat microglia from mice lacking G(i)-coupled P2Y(12) receptors exhibit normal baseline motility but a
72 idges linking its extracellular domains, the P2Y(12) receptor has 2 free cysteines in its extracellul
79 ently identified functional effector for the P2Y12 receptor, in the regulation of ADP-induced TXA2 ge
80 ls of inhibition of platelet aggregation via P2Y(12) receptor inhibition, not only for the prevention
82 stenting and treatment strategies to improve P2Y12 receptor inhibition in patients with high post-tre
83 phoprotein phosphorylation levels to measure P2Y12 receptor inhibition were determined (n = 20) and c
88 me (ACS) patients are not pre-treated with a P2Y12 receptor inhibitor, and percutaneous coronary inte
91 after discharge for beta-blockers, platelet P2Y12 receptor inhibitors, statins, and angiotensin-conv
96 osine diphosphate (ADP)-reactive purinergic (P2Y12) receptor is required for LTE4-mediated pulmonary
97 Because clopidogrel antagonizes the platelet P2Y12 receptor, it is widely prescribed for patients wit
100 nts, but had no effect on Cys17Ser/Cys270Ser P2Y(12) receptor-mediated inhibition of adenylyl cyclase
103 , and/or ATP; (iii) the activation of P2X(1)/P2Y(12) receptors on adjacent PLTs; and (iv) the recursi
104 signaling, via selective stimulation of the P2Y(12) receptor or alpha(2A)-adrenergic receptor, respe
105 ntial signalling and cell activation through P2Y12 receptor or receptor heterodimers but no specific
107 ding motif of the platelet G protein-coupled P2Y(12) receptor (P2Y(12)R) is required for effective re
110 Ticagrelor is a potent antagonist of the P2Y12 receptor (P2Y12R) and consequently an inhibitor of
111 ed BSM contraction is blocked by a selective P2Y12 receptor (P2Y12R) antagonist, PSB 0739 (25 muM), b
114 th tests measuring the adenosine diphosphate-P2Y12 receptor pathway, without significant variations i
116 elated factors (higher on-treatment platelet P2Y12 receptor reactivity and premature thienopyridine d
119 ene adenosine 5'-triphosphate (AR-C67085), a P2Y12 receptor-selective antagonist, and adenosine-2'-ph
120 inhibited in the presence of AR-C69931MX, a P2Y12 receptor-selective antagonist, or GF 109203X, a pr
121 or that abolishes secretion, or AR-C66096, a P2Y12 receptor-selective antagonist; alpha-thrombin-indu
126 in undergoes synergy with ADP acting via the P2Y12 receptor whereas there is no synergy via the P2Y1
127 ructed a chimeric hemagglutinin-tagged human P2Y(12) receptor with its C terminus replaced by the cor
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