3.4.21.68: t-Plasminogen activator
This is an abbreviated version!
For detailed information about t-Plasminogen activator, go to the full flat file.
Word Map on EC 3.4.21.68
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3.4.21.68
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pai-1
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stroke
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inhibitor-1
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artery
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thrombolysis
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fibrinolysis
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endothelial
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infarct
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phorbol
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hemorrhage
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urokinase
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fibrin
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coronary
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clot
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myocardial
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coagulation
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cerebral
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12-o-tetradecanoylphorbol-13-acetate
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fibrinogen
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occlusion
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bleeding
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platelet
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reperfusion
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heparin
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venous
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pkc
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urokinase-type
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upa
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13-acetate
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anticoagulant
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embolism
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thrombus
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intracranial
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willebrand
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angiography
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thrombotic
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recanalization
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streptokinase
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hemostatic
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prothrombin
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d-dimers
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thromboembolic
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patency
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endovascular
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intra-arterial
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antithrombin
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angioplasty
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thrombomodulin
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prothrombotic
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hypercoagulable
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drug development
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diagnostics
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medicine
- 3.4.21.68
- pai-1
- stroke
- inhibitor-1
- artery
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thrombolysis
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fibrinolysis
- endothelial
- infarct
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phorbol
- hemorrhage
- urokinase
- fibrin
- coronary
- clot
- myocardial
- coagulation
- cerebral
- 12-o-tetradecanoylphorbol-13-acetate
- fibrinogen
- occlusion
- bleeding
- platelet
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reperfusion
- heparin
- venous
- pkc
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urokinase-type
- upa
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13-acetate
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anticoagulant
- embolism
- thrombus
- intracranial
- willebrand
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angiography
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thrombotic
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recanalization
- streptokinase
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hemostatic
- prothrombin
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d-dimers
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thromboembolic
-
patency
-
endovascular
-
intra-arterial
- antithrombin
-
angioplasty
- thrombomodulin
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prothrombotic
-
hypercoagulable
- drug development
- diagnostics
- medicine
Reaction
Specific cleavage of Arg-/-Val bond in plasminogen to form plasmin =
Synonyms
Alteplase, BAT-PA, desmoteplase, DSPA beta, DSPA gamma, EC 3.4.21.31, EC 3.4.99.26, human tissue-type plasminogen activator, IV t-PA, IV tissue plasminogen activator, More, plasminogen activator, Plasminogen activator, tissue-type, PLAT, r-tPA, recombinant tissue plasminogen activator, Reteplase, rt-PA, rtPA, sc-tPA, sctPA, single chain enzyme tPA, t-PA, t-PA protein, t-plasminogen activator, tc-tPA, tctPA, Tissue plasminogen activator, tissue type plasminogen activator, tissue-plasminogen activator, Tissue-type plasminogen activator, tissue-type plasmiongen activator, tPA, two chain tPA
ECTree
3.4.21.68 t-Plasminogen activatorAdvanced search results
results (
results (Inhibitors
Inhibitors on EC 3.4.21.68 - t-Plasminogen activator
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INHIBITOR 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
IMAGE
2-([6-[(3'-carbamimidoylbiphenyl-3-yl)oxy]-3,5-difluoro-4-methylpyridin-2-yl]oxy)-4-(dimethylamino)benzoic acid
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2-[(6-[[3'-(aminomethyl)biphenyl-3-yl]oxy]-3,5-difluoropyridin-2-yl)oxy]-4-methylbenzoic acid
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2-[(6-[[5-amino-3'-(aminomethyl)biphenyl-3-yl]oxy]-3,5-difluoropyridin-2-yl)oxy]-4-methylbenzoic acid
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4-(2-aminoethoxy)-N-[3-chloro-2-ethoxy-5-(piperidin-1-yl)phenyl]-3,5-dimethylbenzamide
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4-[(E)-(5-oxo-2-phenyl-1,3-oxazol-4(5H)-ylidene)methyl]benzenecarboximidamide
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6-methoxy-N-(3'-(trifluoromethyl)biphenyl-4-yl)naphthalene-2-sulfonamide
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bis[(phenylamino)acetyl] [2-(4-carbamimidamidophenyl)-1-[(methoxycarbonyl)amino]ethyl]phosphonate
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bivalirudin
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does not exert any protective effect when added at concentrations of 20-200 microg/ml (cell viability of 51.8%)
Cell/platelet-type plasminogen activator inhibitor
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from bovine aortic endothelial
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Chi-tPA 1
specific aptamers are designed using SELEX method, possesses high affinity for the chimeric mutant enzyme
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Chi-tPA 2
specific aptamers are designed using SELEX method, possesses good affinity for the chimeric mutant enzyme
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Chi-tPA 3
specific aptamers are designed using SELEX method, possesses good affinity for the chimeric mutant enzyme
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Chi-tPA 4
specific aptamers are designed using SELEX method, possesses good affinity for the chimeric mutant enzyme
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Chi-tPA 5
specific aptamers are designed using SELEX method, possesses good affinity for the chimeric mutant enzyme
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diphenyl [2-(4-carbamimidamidophenyl)-1-[(methoxycarbonyl)amino]ethyl]phosphonate
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ethyl 4-(3-carbamimidoyl-N-[[2,4,6-tri(propan-2-yl)phenyl]sulfonyl]-L-phenylalanyl)piperazine-1-carboxylate
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Glu-Gly-Arg-chlormethylketone
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directly binds to the catalytic site of tPA. 100 microg/ml given before tPA exposure, reduces cell death (cell viability of 80.5%)
H89
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inhibits dibutyryl-cAMP-mediated changes in tPA activity without affecting metalloproteinase-9 activity
lipopolysaccharide
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decreases tPA activity. Co-treatment with dibutyryl-cAMP and lipopolysaccharide dose-dependently prevents lipopolysaccharide-induced downregulation of tPA activity
N-((2-(iodoacetoxy)ethyl)-N-methyl)amino-7-nitrobenz-2-oxa-3-diazole
P9 plasminogen activator inhibitor-1
N-(4-(aminomethyl)phenyl)-6-carbamimidoyl-2-naphthamide trifluoro acetate
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PAI-1
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ethanol can downregulate the expression of PAI-1, a main inhibitor of tPA in the CNS
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Phe-Pro-Arg-chlormethylketone
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directly binds to the catalytic site of tPA. 100 microg/ml given before tPA exposure, reduces cell death (cell viability of 85.7%)
plasminogen
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substrate inhibition, at low concentrations of t-PA and D-dimer of fibrin containing the D-domain of fibrin in the presence of physiological concentrations of plasminogen
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plasminogen activator inhibitor type 2
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can inhibit cell-bound tPA activity in vitro and thus prevents plasmin formation. Plasminogen activator inhibitor type 2 prevents annexin II heterotetramer/tPA-mediated plasminogen activation by its classic serpin inhibitory activity rather than through competition with tPA/plasminogen for binding. It inhibits cell bound tPA-induced plasmin activity in both an annexin II heterotetramer-dependent and -independent manner
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plasminogen activator inhibitor type-1
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major inhibitor of tissue-type plasminogen activator in the blood
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plasminogen activator inhibitor-1 (PAI-1)
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sctPA is more susceptible to PAI-1 in buffer solution and in the presence of fibrinogen. In the presence of fibrin there is no difference between single-chain enzyme tPA (sctPA) and two chain tPA (tctPA)
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plasminogen activator inhibitor-I
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rapidly inactivates the catalytic activity of tPA in the blood stream
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propanolol
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in normotensive subjects, t-PA release by epinephrine is abolished in the presence of propanolol (10 microg/100 ml per minute). In essential hypertensive patients, the response to isoproterenol is impaired as compared with normotensive subjects and is unaffected by NG-monomethyl-L-arginine coinfusion
Rp-cAMP
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inhibits dibutyryl-cAMP-mediated changes in tPA activity without affecting metalloproteinase-9 activity
serpin plasminogen activator inhibitor (PAI)-1
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primary physiological inhibitor
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transforming growth factor-beta1
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partially inhibits interleukin-1alpha induced expression of tPA mRNA in a dose-dependent manner, maximal inhibition at 60 ng/ml
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Aprotinin
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mitigates tPA-induced neuronal injury. Pre-treatment of N27 cells with aprotinin for 30 min before tPA exposure is protective against cell death, increasing the cell viability to 91.8% at a tPA concentration of 20 microg/ml. When aprotinin treatment follows tPA exposure, cell death is proportional to the length of tPA exposure
Human plasminogen activator inhibitors
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after treatment with 0.01% SDS, active PAI-1 is converted to an inactive form that does not form complexes with PA, after treatment with 0.1% SDS, PAI-1 loses its inhibitory activity and is cleaved as a substrate in the reactive centre; PAI-1
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Human plasminogen activator inhibitors
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and PAI-1 mutant containing substitutions at the P1 and P1' positions; PAI-1
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Human plasminogen activator inhibitors
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PAI-1; PAI-1 may occur in three interconvertible conformations: latent, inhibitor and substrate
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Human plasminogen activator inhibitors
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inhibits the fibrin binding of both the single chain and two chain forms of tPA; PAI-1
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Human plasminogen activator inhibitors
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PAI-1; purification and characterization of recombinant rabbit plasminogen activator inhibitor-1 expressed in Saccharomyces cerevisiae
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Human plasminogen activator inhibitors
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PAI-1; PAI-2 (biochemical characterization)
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plasminogen activator inhibitor 1
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PAI-1, specific endogenous inhibitor, in vivo, administration of mesenchymal stromal cells to mice subjected to middle cerebral artery occlusion significantly increases activation of tPA and downregulates PAI-1 levels in the ischemic boundary zone compared with control PBS treated mice, concurrently with increases of myelinated axons and synaptophysin
plasminogen activator inhibitor type 1
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pregnant women have higher plasma plasminogen activator inhibitor type 1 antigen concentrations that result in lower basal t-PA/plasminogen activator inhibitor type 1 ratios and plasma t-PA activity concentrations
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plasminogen activator inhibitor type 1
an important inhibitor of plasminogen activators
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plasminogen activator inhibitor-1
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is the major inhibitor of tPA-plasminogen signaling. Evidence for an association between plasminogen activator inhibitor-1 and cardiovascular disease pathogenesis
plasminogen activator inhibitor-1
PAI-1, the recombinant chimeric t-PA/b-PA mutant enzyme is 44% less sensitive compared to wild-type tissue plasminogen activator, t-PA
plasminogen activator inhibitor-1
PAI-1, endogenous PAI-1 inactivates the enzyme. Physiologically, PAI-1 inhibits plasminogen activators rapidly and irreversibly, PAI-1 inhibitory mechanism. Analysis of the overall structure of tPA-PAI-1 Michaelis complex, structure-function relationship, overview. The PAI-1 reactive center loop adopts a unique kinked conformation, and on the tPA side, the S2 and S1beta pockets open up to accommodate PAI-1. The deterined crystal structure provides detailed interactions between tPA 37- and 60-loops with PAI-1, overview Comparison to urokinase-type plasminogen activator (uPA, EC 3.4.21.73) structure with bound plasminogen activator inhibitor-1. As a result of the complex formation, an interface of 1202 A2 (solvent-inaccessible area) between PAI-1 and tPA-SPD is formed, which is higher than that of the uPA-SPDx02PAI-1 complex (1058 A2). Of the total area of PAI-1, 8% is involved in interacting with tPA, whereas for uPA, only 6.9% is at the interface. As a protease inhibitor, PAI-1 is very specific to tPA and uPA. Analysis of PAI-1 mutant 14-1B (N150H/K154T/Q319L/M354I)
plasminogen activator inhibitor-1
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plays a major role in the regulation of tPA activity
plasminogen activator inhibitor-1
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PAI-1, astrocyte-derived, induction of PAI-1 by lipopolysaccharide stimulation in astrocytes
plasminogen activator inhibitor-1
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PAI-1, endogenous inhibitor of tPA in the cell
xenon
intraischemic xenon dose-dependently inhibits tissue-type plasminogen activator-induced thrombolysis and subsequent reduction of ischemic brain damage, postischemic xenon virtually suppresses ischemic brain damage and tissue-type plasminogen activator-induced brain hemorrhages and disruption of the blood-brain barrier, therefore xenon should not be administered before or together with a tissue-type plasminogen activator therapy
xenon
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intraischemic xenon dose-dependently inhibits tissue-type plasminogen activator-induced thrombolysis and subsequent reduction of ischemic brain damage, postischemic xenon virtually suppresses ischemic brain damage and tissue-type plasminogen activator-induced brain hemorrhages and disruption of the blood-brain barrier, therefore xenon should not be administered before or together with a tissue-type plasminogen activator therapy
additional information
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stimulation of tPA-mediated plasminogen activity by beta2-glycoprotein I is inhibited by monoclonal anti-beta2GPI antibodies as well as by anti-beta2GPI antibodies from patients with antiphospholipid syndrome. Binding to beta2-glycoprotein I is competitively inhibited by fluid-phase tPA
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additional information
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inhibition of NO synthase with NG-monomethyl-L-arginine (100 microg/100 ml per minute) infusion blunts epinephrine-induced t-PA release in normotensive subjects but not in essential hypertensive patients. In normotensive subjects, t-PA release by epinephrine is not affected by phentolamine coinfusion
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additional information
synthesis and evaluation of a series of naphthamide and naphthalene sulfonamides as enzyme inhibitors containing non-basic groups as substitute for amidine or guanidine groups, overview
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additional information
no inhibition of cleavage of the N-methyl-D-aspartate receptor NR2B domain by alpha2-antiplasmin, but by a commercial tissue plasminogen activator inhibitor
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additional information
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no inhibition of cleavage of the N-methyl-D-aspartate receptor NR2B domain by alpha2-antiplasmin, but by a commercial tissue plasminogen activator inhibitor
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additional information
screening of a peptide aldehyde library against tPA, inhibitory potencies of compounds at 0.01 mM, analysis of effects of different amino acids on positions P4, P3, P2, and P1, overview
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