PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 2510823-3 1989 The affinity for binding the lysine derivatives 6-aminohexanoic acid and N-acetyllysine methyl ester was about equal, suggesting that t-PA does not prefer C-terminal lysine residues for binding. Aminocaproic Acid 48-68 plasminogen activator, tissue type Homo sapiens 134-138 30722079-10 2019 Blocking fibrin polymerization resulted in similar level of NET release seen in tPA-treated clots, whereas epsilon-aminocaproic acid abolished the NET-enhancing effect of tPA. Aminocaproic Acid 107-132 plasminogen activator, tissue type Homo sapiens 171-174 33212896-1 2020 Current antifibrinolytic agents reduce blood loss by inhibiting plasmin active sites (e.g., aprotinin) or by preventing plasminogen/tissue plasminogen activator (tPA) binding to fibrin clots (e.g., epsilon-aminocaproic acid and tranexamic acid); however, they have adverse side effects. Aminocaproic Acid 198-223 plasminogen activator, tissue type Homo sapiens 162-165 2555642-3 1989 t-PA (1 to 100 micrograms/ml) decreased f-MLP-induced chemotaxis and ionophore A23187-induced superoxide and LTB4 release in isolated neutrophils, and these effects were not blocked by the plasmin-inhibitor epsilon-aminocaproic acid (epsilon-ACA). Aminocaproic Acid 207-232 plasminogen activator, tissue type Homo sapiens 0-4 2555642-3 1989 t-PA (1 to 100 micrograms/ml) decreased f-MLP-induced chemotaxis and ionophore A23187-induced superoxide and LTB4 release in isolated neutrophils, and these effects were not blocked by the plasmin-inhibitor epsilon-aminocaproic acid (epsilon-ACA). Aminocaproic Acid 234-245 plasminogen activator, tissue type Homo sapiens 0-4 3146348-1 1988 The activation of human [Glu1]plasminogen [( Glu1]Pg) by human recombinant (rec) two-chain tissue plasminogen activator (t-PA) is inhibited by Cl-, at physiological concentrations, and stimulated by epsilon-aminocaproic acid (EACA), as well as fibrin(ogen). Aminocaproic Acid 199-224 plasminogen activator, tissue type Homo sapiens 63-125 3146348-1 1988 The activation of human [Glu1]plasminogen [( Glu1]Pg) by human recombinant (rec) two-chain tissue plasminogen activator (t-PA) is inhibited by Cl-, at physiological concentrations, and stimulated by epsilon-aminocaproic acid (EACA), as well as fibrin(ogen). Aminocaproic Acid 226-230 plasminogen activator, tissue type Homo sapiens 63-125 12658774-4 2002 Ann-II-mediated enhancement of t-PA-dependent PLG activation was inhibited by epsilon-aminocaproic acid or by pretreatment of Ann-II with carboxypeptidase B with the inhibitive rate being 77.8% and 77.0%, respectively. Aminocaproic Acid 78-103 plasminogen activator, tissue type Homo sapiens 31-35 14743974-1 2003 Studies were conducted on the mechanism of the stimulatory effect of 6-aminohexanoic acid (6-AH) during the in vitro activation of human glutamic plasminogen (Glu-Plg) by streptokinase or by tissue plasminogen activator (t-PA) and the possible role of the addition of physiological concentrations of NaCl to the buffer solution. Aminocaproic Acid 69-89 plasminogen activator, tissue type Homo sapiens 191-225 14743974-1 2003 Studies were conducted on the mechanism of the stimulatory effect of 6-aminohexanoic acid (6-AH) during the in vitro activation of human glutamic plasminogen (Glu-Plg) by streptokinase or by tissue plasminogen activator (t-PA) and the possible role of the addition of physiological concentrations of NaCl to the buffer solution. Aminocaproic Acid 91-95 plasminogen activator, tissue type Homo sapiens 191-225 28007568-8 2017 tPA-catalysed plasminogen activation was markedly inhibited by HA, both in free solution and on the surface of fibrin clots, in the presence and in the absence of 6-aminohexanoate suggesting a kringle-independent mechanism. Aminocaproic Acid 163-179 plasminogen activator, tissue type Homo sapiens 0-3 12738809-4 2003 The generation of cell-bound plasmin mediated by tissue-type plasminogen activator (t-PA), constitutively expressed by VSMCs, requires binding of plasminogen to the cell surface and is inhibited by epsilon-aminocaproic acid (IC50=0.9+/-0.2 mM), a competitor of plasminogen binding to membrane glycoproteins. Aminocaproic Acid 198-223 plasminogen activator, tissue type Homo sapiens 49-82 12738809-4 2003 The generation of cell-bound plasmin mediated by tissue-type plasminogen activator (t-PA), constitutively expressed by VSMCs, requires binding of plasminogen to the cell surface and is inhibited by epsilon-aminocaproic acid (IC50=0.9+/-0.2 mM), a competitor of plasminogen binding to membrane glycoproteins. Aminocaproic Acid 198-223 plasminogen activator, tissue type Homo sapiens 84-88 11112095-3 2000 Fucoidan-Sepharose also showed a high affinity for t-PA, which was largely reversed by 0.002 M 6-aminohexanoic acid (6-AH). Aminocaproic Acid 95-115 plasminogen activator, tissue type Homo sapiens 51-55 11112095-3 2000 Fucoidan-Sepharose also showed a high affinity for t-PA, which was largely reversed by 0.002 M 6-aminohexanoic acid (6-AH). Aminocaproic Acid 117-121 plasminogen activator, tissue type Homo sapiens 51-55 8869642-11 1995 Indeed, lysine analogue (epsilon-amino-caproic acid) sensitive binding of isolated t-PA kringle 2 domain to u-PA could be observed. Aminocaproic Acid 25-51 plasminogen activator, tissue type Homo sapiens 83-87 9836589-5 1998 The stimulation of t-PA-dependent activation of [Glu]plasminogen by the p11 subunit was Ca2+-independent and inhibited by epsilon-aminocaproic acid. Aminocaproic Acid 122-147 plasminogen activator, tissue type Homo sapiens 19-23 7759476-1 1995 To describe the role of the lysyl binding site in the interaction of tissue-type plasminogen activator (t-PA, FGK1K2P) with a forming fibrin clot, we performed binding experiments with domain deletion mutants GK1K2P, K2P, and the corresponding point mutants lacking the lysyl binding site in the absence and the presence of epsilon-amino caproic acid (EACA). Aminocaproic Acid 324-350 plasminogen activator, tissue type Homo sapiens 69-102 8533120-3 1995 During t-PA activation of Glu-Plg, a high degree of synergism was observed between 6-AH and fucoidan while the enhancement by CNBr-Fbg was not influenced by fucoidan and was reversed by 6-AH. Aminocaproic Acid 83-87 plasminogen activator, tissue type Homo sapiens 7-11 8533120-3 1995 During t-PA activation of Glu-Plg, a high degree of synergism was observed between 6-AH and fucoidan while the enhancement by CNBr-Fbg was not influenced by fucoidan and was reversed by 6-AH. Aminocaproic Acid 186-190 plasminogen activator, tissue type Homo sapiens 7-11 8533120-6 1995 The results are interpreted to suggest that CNBr-Fbg and 6-AH compete with each other for the same lysine binding sites (LBS) on the Plg molecule while fucoidan acted synergistically with 6-AH in enhancing the t-PA activation of Glu-Plg by a different mechanism. Aminocaproic Acid 57-61 plasminogen activator, tissue type Homo sapiens 210-214 8533120-6 1995 The results are interpreted to suggest that CNBr-Fbg and 6-AH compete with each other for the same lysine binding sites (LBS) on the Plg molecule while fucoidan acted synergistically with 6-AH in enhancing the t-PA activation of Glu-Plg by a different mechanism. Aminocaproic Acid 188-192 plasminogen activator, tissue type Homo sapiens 210-214 7759476-1 1995 To describe the role of the lysyl binding site in the interaction of tissue-type plasminogen activator (t-PA, FGK1K2P) with a forming fibrin clot, we performed binding experiments with domain deletion mutants GK1K2P, K2P, and the corresponding point mutants lacking the lysyl binding site in the absence and the presence of epsilon-amino caproic acid (EACA). Aminocaproic Acid 352-356 plasminogen activator, tissue type Homo sapiens 69-102 7721771-7 1995 This intermolecular interaction was strongly inhibited by epsilon-aminocaproic acid indicating that the lysine binding site of tPA is involved. Aminocaproic Acid 58-83 plasminogen activator, tissue type Homo sapiens 127-130 8063741-11 1994 Annexin-II-mediated enhancement of t-PA-dependent plasminogen activation was 90-95% inhibited by epsilon-aminocaproic acid or by pretreatment of Ann-II with carboxypeptidase B, indicating a carboxyl-terminal lysine-dependent interaction. Aminocaproic Acid 97-122 plasminogen activator, tissue type Homo sapiens 35-39 1309292-1 1992 We have generated site-specific mutants of the kringle 2 domain of tissue-type plasminogen activator [( K2tPA]) in order to identify directly the cationic center of the protein that is responsible for its interaction with the carboxyl group of important omega-amino acid effector molecules, such as epsilon-amino caproic acid (EACA). Aminocaproic Acid 327-331 plasminogen activator, tissue type Homo sapiens 67-100 7804168-8 1994 t-PA binding could be reduced about 40% by the addition of 10 mmol l-1 of the lysine analogue epsilon-aminocaproic acd (EACA) whereas no inhibitory effect could be demonstrated with arginine. Aminocaproic Acid 120-124 plasminogen activator, tissue type Homo sapiens 0-4 1326962-8 1992 The binding of 125I-t-PA to endothelial cells was reduced in the presence of an excess amount of t-PA, plasminogen and 6-aminohexanoic acid, indicating that the binding sites were also recognized by plasminogen, and that t-PA and plasminogen were bound via lysine binding sites in the molecule. Aminocaproic Acid 119-139 plasminogen activator, tissue type Homo sapiens 20-24 8073394-1 1994 The lysine analogues epsilon-aminocaproic acid (EACA) and trans-4-amino-methyl cyclohexane carboxylic acid (AMCA) are used to prevent excessive bleeding in patients with coagulopathies, such as hemophilia and thrombocytopenia, or in those who have received tissue plasminogen activator (t-PA). Aminocaproic Acid 21-46 plasminogen activator, tissue type Homo sapiens 257-291 8073394-1 1994 The lysine analogues epsilon-aminocaproic acid (EACA) and trans-4-amino-methyl cyclohexane carboxylic acid (AMCA) are used to prevent excessive bleeding in patients with coagulopathies, such as hemophilia and thrombocytopenia, or in those who have received tissue plasminogen activator (t-PA). Aminocaproic Acid 48-52 plasminogen activator, tissue type Homo sapiens 257-291 8112348-6 1994 The binding of t-PA to fibrin and to immobilized FCB-2 was partially inhibited by the lysine analogue 6-aminohexanoic acid (Ki = 123 +/- 47 microM and 364 microM, respectively) but was not modified by carboxypeptidase B, thus indicating involvement of internal lysine residues. Aminocaproic Acid 102-122 plasminogen activator, tissue type Homo sapiens 15-19 8112348-9 1994 Altogether, these data indicate that the mechanism of binding of t-PA to fibrin involves mainly a lysine-independent interaction with the D region which is contributed by sequences present in FCB-5 and FCB-2; contribution to binding by a lysine-dependent interaction was detected only in FCB-2 and is probably of minor relevance as suggested by the limited effect of 6-aminohexanoic acid. Aminocaproic Acid 367-387 plasminogen activator, tissue type Homo sapiens 65-69 1525179-2 1992 We have shown that t-PA dissociates from 1-3-1 in the presence of the lysine analogue 6-aminohexanoic acid (6-AHA). Aminocaproic Acid 86-106 plasminogen activator, tissue type Homo sapiens 19-23 1525179-2 1992 We have shown that t-PA dissociates from 1-3-1 in the presence of the lysine analogue 6-aminohexanoic acid (6-AHA). Aminocaproic Acid 108-113 plasminogen activator, tissue type Homo sapiens 19-23 1525179-4 1992 The yield of t-PA (antigen or total protein) from a 1-3-1-Sepharose column, when eluted using a buffer supplemented with 0.2 M 6-AHA at neutral pH, was as effective as other buffers that involve a strong pH-change, i.e., pH 2-3. Aminocaproic Acid 127-132 plasminogen activator, tissue type Homo sapiens 13-17 1525179-5 1992 However, the enzymatic activity of the t-PA purified with 6-AHA was 25 to 30% higher, as compared with t-PA eluted using a pH change. Aminocaproic Acid 58-63 plasminogen activator, tissue type Homo sapiens 39-43 1525179-6 1992 This resulted in a markedly higher specific activity of t-PA purified with 0.2 M 6-AHA, as compared with t-PA purified using a strong pH-change. Aminocaproic Acid 81-86 plasminogen activator, tissue type Homo sapiens 56-60 1909331-5 1991 In purified systems, both t-PA and plasminogen bound to immobilized amphoterin, and their binding was inhibited by the lysine analogue epsilon-aminocaproic acid. Aminocaproic Acid 135-160 plasminogen activator, tissue type Homo sapiens 26-30 2145980-9 1990 The stimulatory effects of fibrin and partially plasmin-degraded fibrin on one-chain t-PA are suppressed by epsilon-aminocaproic acid and by a monoclonal antibody directed against the lysine binding site of t-PA. Aminocaproic Acid 108-133 plasminogen activator, tissue type Homo sapiens 85-89