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:3.4.21.4 (trypsin)
42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the mechanisms of platelet activation by sublines exhibiting different metastatic potential of two murine experimental tumors: sublines M4 and M9 of the benzopyrene-induced mFS6 sarcoma and sublines B77-AA6 and B77-3T3 of RSV-transformed BALB/c 3T3 fibroblasts. The neoplastic cells of both models induced platelet aggregation, secretion and prostaglandin biosynthesis. In the first model but not in the second, all these processes correlated with the in vivo malignancy of cells. Pretreatment of B77-AA6 and B77-3T3 cells with apyrase significantly decreased platelet aggregation, while pretreatment of M4 cells was ineffective. However, pretreatment with trypsin or neuraminidase was effective in reducing platelet aggregation induced by M4 cells, but not that induced by any of the others; furthermore, phospholipase A2 reduced the platelet response by all sublines. Finally, platelet-activating activity was also found in the pellets obtained following centrifugation of culture media. These results suggest that platelets are stimulated by cancer cells through different mechanisms; platelet activation by a sialo-lipo-protein complex of the cellular membrane was found to be characteristic of the model in which the platelet-aggregating activity of neoplastic cells correlated with their in vivo metastatic behavior.
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PMID:Characterization of the platelet-aggregating activity of cancer cells with different metastatic potential. 373 62

The properties of the specific binding of the muscarinic receptor ligands [3H]quinuclidinyl benzilate and N-[3H]methylscopolamine in rat brain were compared. The specific binding of both ligands was affected equally by heat, phospholipase A2 and trypsin. N-[3H]methylscopolamine labeled only a fraction of the total muscarinic receptors recognized by [3H]quinuclidinyl benzilate in different brain areas and in the heart. Evidence is presented that N-[3H]methylscopolamine, in fact, binds to a subpopulation of [3H]quinuclidinyl benzilate binding sites. The distribution of the high-affinity binding sites of N-[3H]methylscopolamine did not show a different tissue dependence as compared to the total receptor population, and did not parallel the distribution of the pirenzepine-sensitive M1 receptor subtype. Similarly, the affinity of both [3H]quinuclidinyl benzilate and N-[3H]methylscopolamine varied from one tissue to another by a maximum of 2-fold. Although (-)-quinuclidinyl benzilate competed for the specific binding of [3H]quinuclidinyl benzilate in different tissues according to the law of mass-action, N-methylscopolamine showed an anomalous interaction with two binding sites. The low-affinity binding sites of N-methylscopolamine showed saturability of [3H]quinuclidinyl benzilate binding and stereoselectivity. When the binding characteristics of these N-methylscopolamine-inaccessible binding sites of [3H]quinuclidinyl benzilate in the brain were investigated further, it was found that N-methylscopolamine bound exclusively with a single low affinity, whereas pirenzepine still interacted with two receptor populations incorporated in these sites. It is concluded from several lines of evidence that the heterogeneity of binding of N-methylscopolamine to muscarinic receptors does not represent an interaction with the muscarinic M1 and M2 receptor subtypes defined by pirenzepine. Thus, the unique binding profile of pirenzepine to muscarinic receptors cannot be explained merely on the basis of its hydrophilic nature.
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PMID:Multiple binding affinities of N-methylscopolamine to brain muscarinic acetylcholine receptors: differentiation from M1 and M2 receptor subtypes. 375 73

Oxidative phosphorylation and Ca2+-transport functions of liver mitochondria were normalized in rats with alloxane diabetes after peroral administration of phytoecdisteroids - ecdisterone and turkesterone (5 mg/kg) or nerobol (10 mg/kg) within 15 days. These drugs normalized the activity of NADH dehydrogenase and succinate dehydrogenase in respiratory chain of mitochondria, increased distinctly stability of the enzymes to the effect of such factors as heating, effect of phospholipase A2 or trypsin.
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PMID:[Comparative study of the effect of ecdysterone, turkesterone and nerobol on the function of rat liver mitochondria in experimental diabetes]. 377 12

The factors causing a decline in renal perfusion were studied in anaesthetized dogs with acute pancreatitis 4 h after the forceful injection of bile into the pancreatic duct. In 11 such dogs, glomerular filtration rate (GFR) decreased by 40.4% from the control state (P less than 0.05), whereas the clearance of para-aminohippurate (CPAH) declined by 50.2%. These changes were associated with a 15.3% decline in cardiac output (P less than 0.05) and a 26.2% fall in plasma volume. Glomerular morphology was entirely normal. When hypovolemia was prevented by infusing homologous plasma over the 4-h period of observation, the normally observed decline in GFR, CPAH, and cardiac output was prevented. The decline in plasma volume, associated with a rising hematocrit and declining plasma protein concentration, and the associated decrement in renal perfusion, could be entirely duplicated by the infusion of trypsin, chymotrypsin, elastase, and phospholipase A2 (but not lipase or amylase) into normal dogs. These perturbations also were prevented by the concurrent infusion of 4% albumin in saline. At 24 h, however, the renal failure became unresponsive to volume replenishment. We conclude that the decline in renal perfusion in dogs at 4 h with acute pancreatitis is entirely due to hypovolemia, induced by the release of specific enzymes from the inflamed gland, which causes the loss of protein-rich plasma from the vascular space.
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PMID:Renal failure in dogs with experimental acute pancreatitis: role of hypovolemia. 378 59

A skeletal muscle factor which activates hepatic branched-chain keto acid dehydrogenase has been described. Since this factor is labile, the present study was designed to stabilize and characterize this factor. The muscle factor was stabilized by the addition of KCl and the protease inhibitor, antipain. Muscle factor activity was localized to the 100,000 g pellet fraction of muscle homogenate. The muscle factor was inactivated following trypsin or phospholipase A2 digestion.
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PMID:Further characterization of a muscle factor which activates hepatic branched-chain ketoacid dehydrogenase. 380 99

Two basic phospholipases A2 (Pa-11 and Pa-13) have been isolated from the venom of an Australian elapid snake, Pseudechis australis (king brown snake). The reduced and S-carboxymethylated phospholipases A2 were digested with trypsin and the resulting peptides were purified by a combination of chromatography on a DEAE-cellulose DE-52 column and gel filtration procedures. Eleven main peptides from Pa-11 and 9 peptides from Pa-13 could account for the amino acid compositions of the respective enzyme molecules. The alignment of the tryptic peptides and unelucidated regions of the amino acid sequences of tryptic peptides were established by the analysis of the peptides obtained by chymotryptic and/or Staphylococcal protease digestions. Each phospholipase A2 consisted of a single chain of 118 amino acid residues, including 14 half-cystine residues. Although Pa-11 is enzymatically 30-times as active as Pa-13 and highly toxic as compared to Pa-13, they are highly homologous in their amino acid sequences. They are also homologous to the enzymes from mammalian pancreas and the other snake venom phospholipases A2, especially to those from snakes belonging to the subfamilies Acanthophiinae and Laticaudinae.
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PMID:Amino acid sequences of phospholipases A2 from the venom of an Australian elapid snake (king brown snake, Pseudechis australis). 388 51

Assay methods for bee venom phospholipase A2 are presented which respond to different aspects of enzymic behaviour and which allow basal activity, fatty acid activation and acyl-group activation to be distinguished. The stability of the enzyme to thiols and proteinases is dramatically increased by activation with the selective acylating agent, oleoyl imidazolide. These results support the model of activation by conformation change. Limited-fixation studies indicate that enzyme conformation is determined by interaction with the substrate. The oleoyl-enzyme is partially inactivated by trypsin, but its electrophoretic mobility is unchanged. This protective effect is highly selective and only one other component of the venom is protected against trypsin by oleoyl imidazolide. Combination of trypsin and thiol treatment produces a large fragment of the activated enzyme which could be used for structural studies of the activation site.
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PMID:Activation of bee venom phospholipase A2 by oleoyl imidazolide produces a thiol- and proteinase-resistant conformation. 389 47

The cascade enterokinase-trypsinogen-prophospholipase A2 lecithin, generating trypsin, phospholipase A2 and lysolecithin, respectively, was studied in vitro using a novel phospholipase A2 assay. The rate of enterokinase catalysed activation of trypsinogen was maximal at 4 mmol/1 glycodeoxycholic acid; higher concentrations of bile salt progressively inhibited enterokinase activity. Net phospholipase A2 activity in reaction mixtures was critically dependent on the trypsin/prophospholipase A2 molar ratio. Lecithin hydrolysis by phospholipase A2 was dependent on the bile salt/lecithin molar ratio and was optimal at 1.25 to 1. The addition of enterokinase to lecithin and bile salt mixtures, containing trypsinogen and prophospholipase A2 at presumed pathophysiological concentrations, resulted in the generation of concentrations of lysolecithin lytic for pancreatic acinar cells within 5 min. These findings would support the concept that the entry of bile containing active enterokinase into the pancreatic duct system in vivo may in some cases be involved in the initiation of necrotising acute pancreatitis in man.
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PMID:The generation of lysolecithin by enterokinase in trypsinogen prophospholipase A2 lecithin mixtures, and its relevance to the pathogenesis of acute necrotising pancreatitis. 390 74

Platelet-aggregating and thrombin-generating activities of B16 and 3LL cells were inhibited by trypsin, phospholipase A2 and by heating, but not by neuraminidase. It was confirmed that the platelet aggregation effect of these cells is due to thrombin generation. The lung-colonizing ability of treated cells injected intravenously was directly proportional to the ability to generate thrombin and to aggregate platelets. These results suggest that B16 and 3LL cells aggregate platelets through thrombin generation probably via their heat-labile surface lipoprotein, and that emboli composed of platelets, fibrin, and tumor cells may aid further the metastatic process.
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PMID:Platelet-aggregating activities of metastasizing tumor cells. IV. Effects of cell surface modification on thrombin generation, platelet aggregation and subsequent lung colonization. 394 Oct 29

After administration of phytoecdisteroids (ecdisterone, turkesterone) at a dose of 5 mg/kg and the anabolic steroid preparation nerobol at a dose of 10 mg/kg into rats with experimental hepatitis caused by CCl4 poisoning, positive alterations were found in activity of the polyenzymatic systems in membranes of liver mitochondria simultaneously with an increase in their stability and resistance to the effect of exogenous factors producing the mitochondria degradation (controlled heating, treatment with phospholipase A2 or trypsin). These alterations, which appear to occur due to development of strong binds between phospholipids and proteins of inner mitochondrial membrane, promoted normalization of the respiratory chain and the outer pathway of electron transport in hepatocytes of rats with hepatitis.
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PMID:[Effect of phytoecdysteroids and steranobols on the activity and stability of membrane-bound enzymes of liver mitochondria in experimental hepatitis]. 395 17


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