Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.21.5 (thrombin)
33,306 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fibrinogen synthesis in rabbits was evaluated following intravenous infusions of stage 3 degradation products of homologous fibrinogen or fibrin, prepared in vitro. Fibrinogen production was measured by determining the rate of appearance of 75SeM into circulating fibrinogen. Fibrinogen synthesis increased threefold after the administration of stage 3 FDP (D and E), dialyzed to remove LMW digestion fragments, In contrast, the fdp obtained by plasminolysis of crosslinked thrombin clots or of noncrosslinked ancrod or thrombin clots failed to enhance basal fibrinogen production. Accelerated fibrinogen production was not accompanied by alterations in haptoglobin concentration or by increased incorporation of 75SeM into haptoglobin. Fibrinogen synthesis was not increased after infusions of FPA and FPB.
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PMID:Regulation of fibrinogen biosynthesis: effect of fibrin degradation products, low-molecular-weight peptides of fibrinogenolysis, and fibrinopeptides A and B. 42 74

Factor V was isolated from human citrate plasma by very mild purification steps. Cryoprecipitation, fractionation with polyethylene glycol 6000, gel filtration of AcA 44 and adsorption of haptoglobin to immobilized hemoglobin were applied successively, resulting in factor V preparations with a specific activity of 14.5 unit/mg. The yield was 28 percent. A molecular weight of 296 000 was determined by gel filtration and the apparent sedimentation constant found by ultracentrifugation in a sucrose gradient was 7.8 S. Parallel experiments with citrate plasma resulted in the same molecular weight and sedimentation constant. Polyacrylamide gel electrophoresis of factor V in the presence or absence of sodium dodecyl sulfate showed a single protein band. Incubation with human thrombin resulted in an 8-fold activation of the purified factor V.
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PMID:Isolation and partial characterization of human factor V. 45 68

Haptoglobin of two different phenotypes (Hp 1-1 and Hp 2-1) dose-dependently (1-4 mg/ml) stimulated the formation of prostaglandin E2 (PGE2) in osteoblast-like cells isolated from neonatal mouse calvarial bones. The degree of stimulation obtained by haptoglobins (4 mg/ml) on PGE2 biosynthesis was in the same range as that caused by bradykinin (1 mumol/l). Pretreatment of osteoblasts with Hp 1-1 or Hp 2-1 (1-4 mg/ml) resulted in a dose-dependent, synergistic potentiation of the stimulatory effect of bradykinin (1 mumol/l) on PGE2 formation. Thrombin (7 U/ml) stimulated PGE2 formation in the osteoblast-like cells by a mechanism that was also synergistically potentiated by haptoglobin (2 mg/ml). These data show that haptoglobin per se stimulates PGE2 biosynthesis in isolated osteoblasts and, in addition, synergistically potentiates the effect of bradykinin and thrombin. Consequently, the enhanced production of haptoglobin seen in different inflammatory processes may contribute to the destruction of bone by inducing the formation of prostanoids capable of stimulating bone resorption.
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PMID:Haptoglobin synergistically potentiates bradykinin and thrombin induced prostaglandin biosynthesis in isolated osteoblasts. 206 74

A family with Bernard-Soulier syndrome (BSS) was investigated with reference to the genetic markers and thrombin reactions. The proband was a 24-year-old man with a life-long history of epistaxis and gingival bleeding. His parents were first cousins; furthermore, his father was born to parents of second cousins. His father also had bleeding tendency and was also diagnosed as having BSS. However, his mother and elder brother were normal. Genetic marker analysis among the family members suggested that the 16th chromosome was associated with the development of BSS, because only the haptoglobin genotype coded on the 16th chromosome was the marker in both the proband and his father. In addition, they both exhibited decreased thrombin-induced platelet aggregation at a low dose, but an almost normal reaction at a high dose of thrombin.
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PMID:[Genetic markers and thrombin reaction in a family of Bernard-Soulier syndrome]. 261 60

We have reported a rapid method for the quantitation of proteins secreted in culture media (F.M. LaDuca, C.V. Dang, and W.R. Bell (1986) Anal. Biochem. 158, 262-267). Using the same method, we observe that serum-free rat hepatocyte cultures exhibited a 100% increase in detectable secreted fibrinogen-antigen in the presence of 1 unit/ml heparin or greater at 24 h of culture. The amount of transferrin, haptoglobin, and albumin detected was unaltered by the presence of heparin. Since heparin is known to affect certain cellular functions, the fates of [35S]methonine-labeled fibrinogen in cell extracts and culture media were examined employing pulse-chase experiments. Labeled intracellular fibrinogen disappeared at similar rates and was initially released into the media in similar amounts in the presence or absence of heparin. At 8 h during the chase, there was a 40-50% reduction in fibrinogen-antigen in spent culture medium lacking heparin. The presence of heparin did not alter the proteolytic degradation of secreted fibrinogen as determined by immunoblotting of spent culture media proteins separated by polyacrylamide gel electrophoresis. In vitro experiments indicate that clotting of fibrinogen by thrombin reduces the amount of immunodetectable fibrinogen. The results indicate that heparin increases the amount of detectable fibrinogen secreted by cultured hepatocytes by preventing clotting and not by stimulating synthesis or secretion or by inhibiting degradation. Hence, it is critically important to include heparin when secreted fibrinogen is quantitated by the method that we have developed.
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PMID:Heparin requirement for the quantitation of fibrinogen production by primary hepatocyte cultures. 339 44

Immunologic analyses of urinary proteins in patients with gestosis and related obstetrical conditions were performed and urinary protein patterns were compared with blood plasma protein patterns. Many kinds of proteins could be detected in urine of patients with gestosis beside albumin. Therefore, "proteinuria" should be chosen to characterise this state instead of the term "albuminuria". Generally speaking, when a total volume of protein contained in urine increases, its types or subfractions also increase in urine. Next to albumin, the most commonly detected proteins in urine of patients with gestosis were transferrin, IgG, inter-alpha-trypsin inhibitor, alpha 1-antitrypsin, IgA, alpha 2-HS-glycoprotein, alpha 1-acid glycoprotein, Gc-globulin, alpha 1-antichymotrypsin, hemopexin, ceruloplasmin, prealbumin, haptoglobin, anti-thrombin III, Cl-inactivator, IgM, and alpha 2-macroglobulin, in the descending order of their occurrence. Proteins that promptly became negative in urine of gestosis patients after delivery were inter-alpha-trypsin inhibitor, IgA, and ceruloplasmin. On the other hand, proteins most apt to persist in urine were albumin, alpha 2-HS-glycoprotein, and IgG. Generally speaking, lower molecular weight proteins were likely to persist in urine after delivery. Simultaneous determination of blood plasma and urinary proteins was performed for 18 kinds or subfractions of protein. A prognostic value of renal protein clearance was discussed.
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PMID:A study on proteins contained in urine of gestosis patients. 641 21

The complete amino acid sequences and the disulfide arrangements of the two chains of human haptoglobin 1-1 were established. The alpha 1 and beta chains of haptoglobin contain 83 and 245 residues, respectively. Comparison of the primary structure of haptoglobin with that of the chymotrypsinogen family of serine proteases revealed a significant degree of chemical similarity. The probability was less than 10(-5) that the chemical similarity of the beta chain of haptoglobin to the proteases was due to chance. The amino acid sequence of the beta chain of haptoglobin is 29--33% identical to bovine trypsin, bovine chymotrypsin, porcine elastase, human thrombin, or human plasmin. Comparison of haptoglobin alpha 1 chain to activation peptide regions of the zymogens revealed an identity of 25% to the fifth "kringle" region of the activation peptide of plasminogen. The probability was less than 0.014 that this similarity was due to chance. These results strongly indicate haptoglobin to be a homolog of the chymotrypsinogen family of serine proteases. Alignment of the beta-chain sequence of haptoglobin to the serine proteases is remarkably consistent except for an insertion of 16 residues in the region corresponding to the methionyl loop of the serine proteases. The active-site residues typical of the serine proteases, histidine-57 and serine-195, are replaced in haptoglobin by lysine and alanine, respectively; however, aspartic acid-102 and the trypsin specificity, residue, aspartic acid-189, do occur in haptoglobin. Haptoglobin and the serine proteases represent a striking example of homologous proteins with different biological functions.
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PMID:Covalent structure of human haptoglobin: a serine protease homolog. 699 77

Esophageal varices were injected with 5% sodium morrhuate and a solution containing thrombin, concentrated dextrose, and cephalothin sodium using the flexible gastroscope with balloon cuff modification. Hematologic and coagulating parameters were checked before and after the procedure to look for evidence of disseminated intravascular coagulation. No effect was noted on hematocrit, hemoglobin, platelet count, haptoglobin, prothrombin time, partial thromboplastin time, fibrinogen, fibrin split products, factor V, or factor VIII. Injection sclerotherapy with currently available solutions appears to have no effect on the systemic coagulation system.
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PMID:Absence of disseminated intravascular coagulation with endoscopic sclerosis of esophageal varices. 708 44

2 patients treated with penicillin and ampicillin, respectively, suffered from haemorrhagic diathesis, haemolysis, cerebral symptoms and renal insufficiency, resembling a haemolytic-uraemic syndrome. Their plasma was red due to the presence during several days of haemoglobin-haptoglobin complexes, the P-haemoglobin being 2.8 and 1.6 g/l, respectively. Coagulation tests showed an unusual pattern with prolonged activated partial thromboplastin times, an extremely long thrombin time and very high levels of fibrinogen degradation products. Repeated transfusion had no effect. The patients were considered to have developed a drug-induced serum sickness associated with insufficient function of the reticuloendothelial system, and secondary to this an accumulation of haemoglobin-haptoglobin complexes in plasma. When the penicillin drugs were discontinued, all measured variables rapidly normalised and the patients recovered completely. Thus, the haemolyticuraemic syndrome seemed to be caused by the serum sickness, possibly via circulating or cell-associated immune complexes. The possibility of a type III allergic reaction should be considered in patients with haemolytic-uraemic-like syndromes.
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PMID:Haemolytic uraemic syndrome and accumulation of haemoglobin-haptoglobin complexes in plasma in serum sickness caused by penicillin drugs. 739 52

Inflammation-induced localized bone resorption in diseases such as marginal and apical periodontitis, rheumatoid arthritis, and osteomyelitis is due to activation and recruitment of osteoclasts by locally produced cytokines and inflammatory mediators. Thus several interleukins (1, 3, 4, 6, and 11), tumor necrosis factors (alpha, beta), colony-stimulating factors (M and GM), leukemia inhibitory factor, gamma-interferon, and transforming growth factor-beta have effects on bone resorption and bone formation in vivo and in vitro. The kallikrein-kinin system and the coagulation cascade are also activated in inflammation. We have found that peptides produced in the kallikrein-kinin system (bradykinin, kallidin) and thrombin, the end product in the coagulation cascade, can stimulate bone resorption in vitro. The stimulatory effect of bradykinin is linked both to B1 and B2 bradykinin receptors. Both kinins and thrombin stimulate prostaglandin biosynthesis in bone parallel with the bone resorptive effect. The stimulatory effect of bradykinin on bone resorption is completely lost when the prostaglandin response is abolished, whereas thrombin can stimulate bone resorption both via prostaglandin-dependent and independent mechanisms. In addition, bradykinin and thrombin act in concert with interleukin-1 to synergistically stimulate bone resorption and prostaglandin biosynthesis. We also have found that one of the acute-phase reactants, haptoglobin, can stimulate bone resorption in vitro, indicating the possibility of generalized bone loss in chronic inflammatory diseases. Moreover, haptoglobin synergistically potentiates bradykinin-induced and thrombin-induced prostanoid biosynthesis in osteoblasts. These observations indicate that the rate of bone resorption in inflammation-induced bone loss may not be due to a single factor but to the concerted action of several local or systemic factors.
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PMID:Regulation of bone metabolism by the kallikrein-kinin system, the coagulation cascade, and the acute-phase reactants. 752 72


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