PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23313628-4 2013 PAR-1 regulation was studied prospectively in 86 consecutive patients with stable coronary artery disease treated with aspirin and clopidogrel (67 patients) or prasugrel (19 patients) and correlated the data to ADP inducible platelet reactivity by impedance aggregometry. Clopidogrel 131-142 coagulation factor II thrombin receptor Homo sapiens 0-5 33093222-1 2021 OBJECTIVE: To investigate the association between protease-activated receptor-1 (PAR-1) gene F2R polymorphisms and efficacy of clopidogrel for minor stroke or TIA. Clopidogrel 127-138 coagulation factor II thrombin receptor Homo sapiens 50-79 33093222-1 2021 OBJECTIVE: To investigate the association between protease-activated receptor-1 (PAR-1) gene F2R polymorphisms and efficacy of clopidogrel for minor stroke or TIA. Clopidogrel 127-138 coagulation factor II thrombin receptor Homo sapiens 81-86 33093222-1 2021 OBJECTIVE: To investigate the association between protease-activated receptor-1 (PAR-1) gene F2R polymorphisms and efficacy of clopidogrel for minor stroke or TIA. Clopidogrel 127-138 coagulation factor II thrombin receptor Homo sapiens 93-96 33093222-6 2021 The association between F2R IVSn-14 A/T polymorphism and clopidogrel response was present regardless of the carrier status of the CYP2C19 loss-of-function alleles. Clopidogrel 57-68 coagulation factor II thrombin receptor Homo sapiens 24-27 33093222-8 2021 CONCLUSIONS: Among patients with minor ischemic stroke or TIA who were receiving clopidogrel and aspirin, those carrying the F2R IVSn-14 T allele had a lower rate of recurrent stroke than those who were not. Clopidogrel 81-92 coagulation factor II thrombin receptor Homo sapiens 125-128 23041015-3 2013 METHODS: The response to agonists specific for protease-activated receptors (PAR)-1 and -4 was tested by multiple electrode impedance aggregometry in 82 patients on stable doses of clopidogrel or prasugrel, and in 55 healthy controls. Clopidogrel 181-192 coagulation factor II thrombin receptor Homo sapiens 47-90 21819272-5 2011 In preclinical and Phase I - II studies, inhibition of thrombin-mediated platelet activation by a PAR-1 inhibitor, in general, has added to the antithrombotic efficacy of aspirin and clopidogrel without increasing bleeding. Clopidogrel 183-194 coagulation factor II thrombin receptor Homo sapiens 98-103 22459907-0 2012 Protease activated receptor-1 (PAR-1) mediated platelet aggregation is dependent on clopidogrel response. Clopidogrel 84-95 coagulation factor II thrombin receptor Homo sapiens 0-29 22459907-0 2012 Protease activated receptor-1 (PAR-1) mediated platelet aggregation is dependent on clopidogrel response. Clopidogrel 84-95 coagulation factor II thrombin receptor Homo sapiens 31-36 22459907-2 2012 Thrombin induces platelet aggregation by binding to protease activated receptor-1 (PAR-1), and inhibition of PAR-1 has been evaluated in patients treated with clopidogrel to reduce ischemic events after acute coronary syndromes. Clopidogrel 159-170 coagulation factor II thrombin receptor Homo sapiens 109-114 22459907-3 2012 Residual PAR-1 mediated platelet aggregation may be dependent on extent of clopidogrel response. Clopidogrel 75-86 coagulation factor II thrombin receptor Homo sapiens 9-14 22459907-9 2012 Addition of PAR-1 antiplatelet drugs may be most effective in patients with reduced clopidogrel response and high residual TRAP mediated platelet aggregation. Clopidogrel 84-95 coagulation factor II thrombin receptor Homo sapiens 12-17 16837456-8 2006 P2Y12 receptor inhibitors clinically in use such as clopidogrel are postulated to decrease platelet aggregation through partial inhibition of PAR1 signaling. Clopidogrel 52-63 coagulation factor II thrombin receptor Homo sapiens 142-146 17303701-8 2007 Given the efficacy of clopidogrel, which blocks the G(i/o)-coupled P2Y purinoceptor 12, as an antiplatelet/antithrombotic drug, our data suggest that specifically blocking only PAR1-mediated G(i/o) signaling could also be an effective therapeutic approach with the possibility of less unwanted bleeding. Clopidogrel 22-33 coagulation factor II thrombin receptor Homo sapiens 177-181 16194864-0 2005 PAR-1 genotype influences platelet aggregation and procoagulant responses in patients with coronary artery disease prior to and during clopidogrel therapy. Clopidogrel 135-146 coagulation factor II thrombin receptor Homo sapiens 0-5 16194864-3 2005 We also determined whether the P2Y12 antagonist clopidogrel could offset any observed functional polymorphism of the PAR-1 receptor by inhibiting P2Y12-mediated amplification of TRAP-induced responses. Clopidogrel 48-59 coagulation factor II thrombin receptor Homo sapiens 117-122 16194864-10 2005 Higher platelet reactivity associated with PAR-1 IVSn-14 A allele homozygotes persists despite clopidogrel therapy. Clopidogrel 95-106 coagulation factor II thrombin receptor Homo sapiens 43-48 34954768-0 2022 Associations of CYP2C19 and F2R genetic polymorphisms with platelet reactivity in Chinese ischemic stroke patients receiving clopidogrel therapy. Clopidogrel 125-136 coagulation factor II thrombin receptor Homo sapiens 28-31 34954768-8 2022 The newly identified rs168753 in F2R gene may influence the efficacy to clopidogrel-aspirin therapy for ischemic stroke patients. Clopidogrel 72-83 coagulation factor II thrombin receptor Homo sapiens 33-36