Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.73 (urokinase-type plasminogen activator)
 10,685 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The fibrinolytic activity in biopsy specimens of superficial veins obtained from postmenopausal women before and after treatment with a nonsteroidal estrogen (P 1496) was determined as well as the coagulation factors antithrombin 3 and components of the fibrinolytic system. Patients were given P 1496, 50 mg/day for 3 weeks before surgery for uterine prolapse. The prothrombin + factor 7 + factor 10 (P and P), factor 8, antithrombin 3, alpha-1-antitrypsin, anti(-2)-macroglobulin, and inhibitors of urokinase induced plasminogen activation were measured. Vein biopsy specimens were taken from the dorsal side of the hand. Fibrinolysis was measured after incubation. The fibrinolytic activity of the specimens was normal and unchanged with treatment.
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PMID:Coagulative and fibrinolytic studies on postmenopausal women treated with a new non-steroidal oestrogen. 7 33

Trypsin, thrombin, fibrinolysin, papain, chymothrypsin and urokinase were immobilized on aminopolystyrene resin by the reaction of diazocoupling. An activation of prothrombin and plasminogen and also hydrolysis of fibrin by immobilized enzymes were studied. The immobilized enzymes hydrolyzed N-benzoyl-1-arginine ethyl ester and L-tyrosine ethyl ester. The only preparation of immobilized thrombin possessed the coagulational activity. After the covalent binding trypsin and plasmin maintained the capacity to cause a fibrinolysis. Immobilized trypsin, plasmin, papain, chymotrypsin and urokinase exhibited the fibrinolytic effect due to convertion of plasminogen into plasmin.
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PMID:[Blood coagulating properties of immobilized proteases]. 14 May 25

A 38-residue fragment is isolated from carboxymethylated plasminogen. Residues 29-38 have the same sequence as the amino-terminal end of the light chain of plasmin. The sequence 1-28 is therefore the sequence of the carboxyl-terminal end of the heavy chain and contains the specific sequence at which urokinase (EC 3.4.99.26) and other plasminogen-activating serine proteases split. Two of the five carboxymethyl-cysteine residues in the isolated fragment are situated close to the cleavage site and the fragment is not itself a substrate for plasminogen-activators. Residues 1-11 show extensive sequence homology with residues 137-147 and 242-252 in prothrombin, which are located in corresponding regions of the two internally homologous 83-residue structures in the non-thrombin part of the molecule, indicating that such structures may be a common feature of the non-protease part of the larger serine protease zymogens.
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PMID:Amino-acid sequence of activation cleavage site in plasminogen: homology with "pro" part of prothrombin. 105 75

The purpose of the study was to explore hemostasis in children suffering from hemorrhagic vasculitis (HV) by means of the new amidolytic methods using chromogenic substrates. The patient's plasma was studied for the content of thrombin, trypsin, factor Xa, AT-III, kallikrein, plasmin, free heparin, urokinase, factor 3 of platelets, prothrombin and Willebrand's factor. 69 children with HV were entered into the study. All of them were examined during crises. In cutaneous HV, the content of trypsin decreased 3-fold, the content of factor Xa increased 5-fold; there was a negligible increase in the plasmin and AT-III levels; the content of kallikrein rose 2-fold, that of urokinase 60-fold; the release of platelet factor 3 was intensified 1.5-fold, the activity of prothrombin 3-fold. These data indicate that in cutaneous HV, blood coagulation increased. However, the signs of disseminated intravascular coagulation were lacking because of the high blood anticoagulant activity. In mixed HV, the phase of hypercoagulation was not made for by the blood anticoagulant activity, since the latter one was depleted. The capillary toxic nephritis may give rise to disseminated intravascular coagulation associated with the depletion of the anticoagulant component. The gravity of HV and its complications can be predicted according to the characteristics of the anticoagulant component of hemostasis, especially according to the levels of urokinase and AT-III.
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PMID:[State of hemostasis in hemorrhagic vasculitis in children]. 151 26

We have examined the changes in fibrinolysis after urokinase administration for 6 patients with acute myocardial infarction. Patients were treated with urokinase with doses between 960,000 and 1,440,000 units, and fibrinolytic activities were determined by using newly developed molecular markers: alpha 2-plasmin inhibitor (alpha 2-PI), plasminogen, alpha 2-PI plasmin complex (PIC) and FDP D dimer. We also used classical hemostatic tests such as prothrombin time (PT) and plasma fibrinogen level. These tests were measured with 1 to 2 hour intervals, during the first 6 hours of therapy, daily during the next 3 days, and subsequently on day 7 and 14. The initial intravenous administration of urokinase with a dose of 460,000 units produced a significant decrease in alpha 2-PI level, but induced only minimal changes in the level of fibrinogen, FDP-E, and FDP D-dimer, suggesting that enhancement of fibrinolytic activity was less pronounced under such therapy. This might be due to the ability of residual amounts of alpha 2-PI to sufficiently inhibit plasmin generation in the circulating blood. However, a subsequent injection of 960,000 units of urokinase into the coronary artery induced a profound reduction in the alpha 2-PI to an unmeasurable level, and resulted in a marked enhancement of fibrinolytic activity. The elevation of FDP-E and FDP D-dimer was accompanied with this decrease in alpha 2-PI and persisted for more than 6 hours after urokinase injection. Prolongation of PT due to decrease in fibrinogen level was also observed over 6 hours.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Serial changes in hemostatic molecular markers after urokinase therapy of acute myocardial infarction]. 153 65

The Kringle-1 structure of plasminogen (PGK-1), the Kringle-2 structure of tissue plasminogen activator (PAK-2) and the Kringle structure of prourokinase (UKK) has been modeled on the basis of the three-dimensional structure of Kringle-1 of prothrombin (PTK-1) at 2.8 A resolution. The predicted three-dimensional structure of these Kringles shows that the binding site of PGK-1 is characterized by an apparent dipolar site, the polar parts of which are separated by a hydrophobic region. PAK-2 possesses the anionic center but has not a cationic binding center which might be provided by a guanidinium group from Arg-69 located adjacent to the Arg-71 position. UKK possesses neither the anionic binding center nor the cationic center which are probably the main reason for the poor fibrin specificity of urokinase.
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PMID:The structural basis of the poor fibrin specificity of urokinase(I)--knowledge-based prediction of kringle structures of urokinase and its related proteins. 158 Oct 2

Thirty-one patients (29 males and 2 females) with 34 thrombosed grafts were treated by direct intra-arterial infusion of urokinase; the lesions were acute in 27 cases and chronic (2-4 months) in 4. Urokinase was infused in doses of 50,000 UI/h. Angiographic follow-up exams were performed every 12 hours. The infusion was stopped when lumen patency was re-established and there was no significant mural thrombus or peripheral embolus. Treatment usually lasted 4-72 hours (average: 18 hours). The hematological status was controlled by measuring plasma fibrinogen, coagulation time, partial thromboplastin time, prothrombin and antiplasmin time. Initial success rate was 76% (23 patients). Overall 1-year patency was 56% in 23 cases: 85% in the patients with correctable lesions by means of surgery or PTA, and 46% in the patients with non-correctable lesions. After the first period, patency remained high in the patients followed up to 5 years. Our experience confirms that lysis of a thrombosed graft is possible by the local infusion of a low-dose fibrinolytic agent and exhibits high success rate and low complication rate in acute and chronic obstructions.
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PMID:[Loco-regional fibrinolysis in peripheral arterial bypasses. Our experience]. 163 28

A recombinant 90-residue polypeptide fragment containing the three-loop kringle-2 domain of human tissue-type plasminogen activator (t-PA) has been studied by two-dimensional 1H-NMR spectroscopy at 500 MHz. Complete sequence-specific resonance assignments were derived. Overall, the kringle exhibits a compact, folded conformation with more than 50% of the residues in irregular structures. Elements of secondary structure were identified from sequential, medium- and long-range dipolar (Overhauser) interproton interactions. These identifications were corroborated by analysis of spin-spin scalar 3J alpha N splittings and identification of backbone amide NH protons exhibiting retarded 1H/2H exchange in 2H2O. Three antiparallel beta-sheets and six tight turns were located. In addition, one short alpha-helical region was found in the Ser43-Ala44-Gln44a-Ala44b-Leu44c-Gly45+ ++ segment; this region contains three-residue insertions unique to the t-PA and urokinase kringles. Although the secondary structure of the t-PA kringle 2 in solution is in overall agreement with that observed in the crystallographic structure of the prothrombin kringle 1 [Tulinsky, A., Park, C.H. & Skrzypczak-Jankun, E. (1988) J. Mol. Biol. 202, 885-901], the alpha-helical segment and other details of the secondary structure differ somewhat from the prothrombin homolog.
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PMID:Kringle-2 domain of the tissue-type plasminogen activator. 1H-NMR assignments and secondary structure. 190 89

Umbilical artery catheterization is known to be associated with aortoiliac thrombosis in approximately 1% of newborns in whom catheters are placed. We describe a case of catheter-associated aortoiliac thrombosis in a newborn who was successfully treated by urokinase infusion. The infant was monitored by imaging studies followed by ultrasonography. The use of real-time ultrasonography enabled us to image this infant's aortoiliac thrombosis in an accurate, noninvasive manner and monitor the effectiveness of thrombolytic therapy. The fibrinolytic state was achieved with a combination of intravenous and intraarterial infusions of urokinase. Frequent measurement of prothrombin time, activated partial thromboplastin time, fibrinogen, and thrombin time was used to guide fibrinolytic therapy. We reviewed the literature for similar cases of aortoiliac thrombosis in newborns; some were managed by medical means, others by operation. The success rate of the two approaches appeared to be approximately equal. Therefore we recommend the less invasive approach first--urokinase therapy--to be followed by surgical intervention if thrombolysis is unsuccessful.
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PMID:Urokinase treatment of neonatal aortoiliac thrombosis caused by umbilical artery catheterization: a case report. 194 79

Thrombin, plasmin and tissue plasminogen activator (one- and two-chain forms) were examined with respect to their reaction with the suicide substrate, 3,4-dihydro-3-benzyl-6-chloromethylcoumarin, at 4 degrees C. The enzymes were irreversibly inhibited and the apparent second-order rate constants ki/Ki were 31,000, 316, 187 and 250 M-1.s-1, respectively. The extent of fibrin clot lysis induced by urokinase and two-chain tissue plasminogen activator was considerably decreased after treatment of these enzymes with the dihydrocoumarin derivative (molar excess of inhibitor over enzyme ranging from 6 to 21 for urokinase and 50 to 1500 for tissue plasminogen activator). This inhibitor has been tested as anticoagulant in human plasma and was effective at prolonging the prothrombin time from 12 to 40 s.
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PMID:Reaction of thrombin and proteinases of the fibrinolytic system with a mechanism-based inhibitor, 3,4-dihydro-3-benzyl-6-chloromethylcoumarin. 213


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