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)

A substance inhibitory to protein synthesis was purified from mouse skeletal muscle by gel filtration and ion-exchange chromatography, as well as by centrifugation on sucrose gradients. The molecular weight of the inhibitor, determined by sodium dodecyl sulphate/polyacrylamide-gel electrophoresis, was 71000. The inhibitory activity was insensitive to ribonuclease A, deoxyribonuclease I and phospholipase C. It was sensitive to Pronase treatment but insensitive to heat-treatment and trypsin degradation. The present results, taken together with previous studies, indicate that the site of action of the inhibitor is not on the initiation phase of protein synthesis but rather at a step after the binding of aminoacyl-tRNA to ribosomes. The increased inhibitor activity found in dystrophic muscle is discussed.
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PMID:Studies of a factor from dystrophic mouse muscle inhibitory towards protein synthesis. 74 60

Comparative investigations on the inhibition of chitin synthetase of Mucor rouxii revealed that in contrast to results obtained in vivo, only few fungicides and other compounds inhibit the enzyme in vitro. Besides the well-known effect of polyoxin D, an inhibition was demonstrated for terrazol, tridemorph, hinosan, and formulated preparations of dimilin (PH 60--40, 60--38). The latter preparations, however, showed growth inhibition also with fungal species which do not synthesize chitin and the pure compounds are ineffective. Inhibition by phospholipase C, unsaturated fatty acids, and the reversibility of the inhibition caused by terrazol after addition of procain-hydrochloride demonstrates that phospholipids are essential for the activity of the enzyme, whereas sterols seem to be ineffective. Action of trypsin, PCNB, pentachlorophenol, and some similar compounds results in significantly increased activity, which in the case of trypsin could be due to the hydrolysis of a protein inhibitor. Hinosan inhibits the enzyme indirectly in a still unexplored manner.
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PMID:[Inhibition of chitin synthetase of Mucor rouxii in vitro by fungicides and other compounds]. 75 46

Low concentrations of protease and trypsin reduced the electrophoretic mobility (EPM) of thymocytes; with higher concentrations it was normal or above. Differences in membrane structure of thymocytes, T and B cells was found as B cells showed no reduction while T cells gave intermediate values. Further the reduction was greater with protease than with trypsin. Formalin fixation increased the EPM of all normal cell types to a similar degree. The EPM of proteolytically treated thymocytes and B cells was increased to a similar level and to a greater degree than neuraminidase-treated thymocytes. Small amounts of sialic acid were detected in the supernatant after proteolytic treatment of thymocytes. Protease reduced the binding of anti-lymphocyte serum, while no definite effect was obtained with trypsin. Neither sublytic doses of phospholipase C nor ribonuclease appeared to change the EPM.
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PMID:Electrophoresis of lymphoid cells. Differences in the cell membrane structure of murine thymocytes, T and B cells revealed by enzyme and formalin treatment. 76 20

The release of beta-lysin, which followed the intravenous injection of antigen-antibody complexes, did not take place when these complexes were added to citrated whole blood but did occur in heparinized blood. beta-Lysin release in heparinized blood was inhibited by citrate but were reversed by the addition of calcium ions that implicated complement reactions. Fourteen different enzymes were added to platelet-rich plasma (PRP). Streptokinase, neuraminidase, papain, phospholipase C, sulfatase, and trypsin caused platelets to release significant quantities of beta-lysin, whereas elastase, phosphatase, protease, ribonuclease A, hyaluronidase, lipase, and pepsin caused little or no increase in the plasma beta-lysin concentration. One enzyme, fibrinolysin, inactivated beta-lysin faster than it was released. The enzyme-induced release of beta-lysin from PRP was often accompanied by a reduction in the number of platelets. The intravenous injection of streptokinase, neuraminidase, and sulfatase caused in vivo releases of beta-lysin into the plasma. The platelet-aggregating substances collagen, arachidonic acid, and adenosine 5'-diphosphate caused beta-lysin to be released from PRP. The platelet-aggregating substances L-epinephrine, zymosan, fibrinogen, reserpine, and serotonin caused little or no release of beta-lysin from platelets. The results of this study indicate that the release of beta-lysin during antigen-antibody-complement reactions, blood coagulation, phagocytosis, and inflammation could be enzyme mediated.
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PMID:Release of beta-lysin from platelets caused by antigen-antibody complexes, purified enzymes, and platelet-aggregating substances. 84 4

1. The properties of rat liver cytoplasmic alpha-tocopherol binding protein have been studied. 2. The binding protein sedimented in the 3 S region of sucrose density gradients, and gel filtration indicated an approximate molecular weight of 30 500. 3. Of the tissues examined by the present assay, binding was detectable only in the liver. 4. Optimal binding was achieved by incubation at 26 degrees C for 4 h and was independent of pH between 7.4 and 9.0. 5. Pronase completely abolished binding. The binding protein was, however, almost completely resistant to trypsin, and unaffected by RNAase, DNAase, triacylglycerol lipase, and phospholipase C. 6. A variety of tocopherol analogues and other lipid-soluble compounds were tested for their ability to compete for binding. Only alpha-tocopherol and to a lesser extent alpha-tocotrienol and gamma-tocopherol exhibited competition. alpha-Tocopherol acetate, alpha-tocopherol quinone and 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid had no effect on binding. 7. Tocopherol binding was reversible, and the tocopherol was not metabolized during incubation.
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PMID:Rat liver alpha-tocopherol binding protein. 87 71

Acid hydrolases from extracts of human blood leucocytes lyse Staph.aureus, Staph.albus and Strep.faecalis in vitro. The leucocyte enzymes can be substituted by a lytic mixture which contains crude trypsin, lysolecithin, phospholipase C and lysozyme, which lyse other bacterial species, e.g. E.coli and Listeria which are resistant to leucocyte enzymes. Bacteriolysis by the lytic agents is strongly inhibited by the anionic polyelectrolytes, heparin, chondroitin sulphate, DNA, dextran sulphate and other sulphated mucopolysaccharides, by the cationic materials, histone, protamine sulphate, leucocyte cationic proteins and polylysine. Other strong inhibitors are trypsan blue and congo red, the phospholipids phosphatidyl serine and ethanolamine, gold thiomalate, extracts of coffee and tea and the anti-inflammatory agents, ultracorten-H, and ultracortenol. Bacteriolysis is also strongly inhibited by normal human serum and by synovial fluids from patients with a variety of joint diseases. The inhibitors in these body fluids are associated with the globulin fractions. Since mixtures of anionic and cationic polyelectrolytes, at equimolar concentrations, failed to inhibit bacteriolysis by leucocyte enzymes, it is postulated that a delicate balance between positively and negatively charged inhibitors control the degradation of cell wall components of bacteria in inflamed areas. Such bacterial components, induce 'storage type' granulomas. The possible role played by polyelectrolytes in the control of the inflammatory process induced by leucocyte hydrolases will be discussed.
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PMID:The interaction of leukocytes and their hydrolases with bacteria in vitro and in vivo: the modification of the bactericidal and bacteriolytic reactions by cationic and anionic macromolecular substances and by anti-inflammatory agents. 94 4

Insulin, a mitogen for cultured chick embryo fibroblasts (Temin, H.M. (1968) Cancer 3, 771-787), has been employed to characterize the effects of mitogen/cell membrane interactions as it relates to growth. The specific binding of 125I-insulin to substratum-attached cells is time- and temperature dependent and is optimum at a pH of 7.0. Fetal calf and chicken sera, somatomedin "A/C mixed," and desalanine or native porcine insulin compete with 125I-insulin for membrane-binding sites. Proinsulin, although competing less effectively than native insulin for binding, is more effective than desoctapeptide insulin. Unrelated polypeptide hormones do not compete for 125I-insulin binding. The lowest concentration of insulin at which specific binding is detected is 0.1 nM. Scatchard plot analysis of the binding data indicates that there are two types of binding sites in confluent cultures of fibroblasts: one of high affinity (K1 = 2 to 6 X 10(8) M-1) and low capacity, the other of low affinity (K2 = 0.8 to 3.0 X 10(7) M-1) and high capacity. Approximately 1.9 and 7.1 X 10(3) molecules of insulin are bound at each site, respectively. A 10-min incubation at 24 degrees of the fibroblasts with 10 mug/ml of trypsin causes a 2-fold stimulation of specific 125I-insulin binding and a similar 2-fold increase in insulin-stimulated 2-deoxy-D-glucose uptake and thymidine incorporation. Neuraminidase treatment also produces a 37% increase in specific 125I-insulin binding but treatment with alpha-chymotrypsin or phospholipase C are without significant effect. The results of this and additional experiments support the hypothesis that trypsin treatment of chick embryo fibroblasts leads to an unmasking of 125I-insulin binding sites. Serum starvation of fibroblasts for 12 or 24 h produces a 2.5- to 5-fold increase in specific 125I-insulin binding. This increase is the result of an increase in the number of hormone-binding sites from 9 X 10(3) to 6 X 10(4) per cell which are predominantly of the low affinity type. There is no change in the affinity constants. The presence of camptothecin, or cordycepin, or cycloheximide in the incubation medium completely blocks the increase in number of 125I-insulin-binding sites resulting from serum starvation. The addition of native insulin to the medium of serum-starved cultures also blocks this increase. The magnitude of insulin-stimulated 2-deoxy-D-glucose uptake and thymidine incorporation correlates with the levels of occupancy of the low affinity 125I-insulin-binding sites in untreated fibroblasts. In fibroblasts cultured in the absence of serum, the marked increase in insulin-stimulated 2-deoxy-D-glucose uptake and thymidine incorporation parallels the increase in number of mitogen receptors. The concentration of insulin that produces a half-maximum stimulation of thymidine incorporation is calculated to be 5 X 10(-8) M. At this concentration of insulin, 42% of the receptor sites are occupied.
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PMID:Mitogen receptors in chick embryo fibroblasts. Kinetics, specificity, unmasking, and synthesis of 125I-insulin binding sites. 98 22

The 5'-nucleotidase localized in rat liver plasma membranes was purified to a single protein, which contained phospholipid. The molecular weight and the sedimentation constant were about 150 000 and 7 S in the presence of sodium deoxycholate, while the enzyme protein was aggregated when the preparation was dialyzed thoroughly. The purified 5'-nucleotidase exhibited the same properties as the 5'-nucleotidase in plasma membranes. The 5'-nucleotidase activity was increased by the addition of various bile salts or by the solubilization of membranes with trypsin, papain or phospholipase C. The solubilized and aggregated forms of the enzyme showed different substrate specificity for nucleotides, pH optimum, heat stability and Km. The purified enzyme catalyzed an exchange reaction between AMP and adenosine, which was diminished by the addition of sodium deoxycholate.
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PMID:Effect of sodium deoxycholate on 5'-nucleotidase. 125 10

The ATP.Mg-dependent type-1 protein phosphatase and its activating factor (protein kinase FA) were identified to exist in brain synaptosome. The inactive protein phosphatase was found to exist in the synaptosomal cytosol whereas its activating factor (protein kinase FA) was present in the synaptosomal membrane, indicating that the inactive protein phosphatase and its activating factor FA are localized in two separate subcellular compartments. The membrane-bound FA was found to exist in two forms; approximately 75% of FA is inactive and trypsin-resistant, whereas 25% of FA is active and trypsin-labile. When membranes were incubated with exogenous phospholipase C, the inactive/trypsin-resistant FA could be activated and sequestered to become the active/trypsin-labile FA in a time- and dose-dependent manner. Taken together, the results provide initial evidence that the activation-sequestration of membrane-bound protein kinase FA may represent one mode of control modulating the activity of protein kinase FA and thereby to activate protein phosphatase in brain synaptosome, representing an efficient regulatory mechanism for regulating neurotransmission in the central nervous system.
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PMID:The mechanism of activation of protein kinase FA (the activator of type-1 protein phosphatase) in brain synaptosomes. 131 12

1. The membrane anchor of aminopeptidase N associated with larval midgut cell membranes of the silkworm, Bombyx mori, was investigated by using phosphatidylinositol-specific phospholipase C (PIPLC) and proteases. 2. Aminopeptidase N, which was virtually all localized in the brush border membrane, was solubilized by PIPLC but not by papain or trypsin. 3. Detergent-solubilized amphiphilic aminopeptidase N was converted into a hydrophilic form by PIPLC but not by papain. 4. Either of these effects of PIPLC on aminopeptidase N was maximally 40%. 5. These results suggest that in larval midgut cells of the silkworm, B. mori, at least 40% aminopeptidase N is anchored in the brush border membrane via glycosyl-phosphatidylinositol.
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PMID:Partial release of aminopeptidase N from larval midgut cell membranes of the silkworm, Bombyx mori, by phosphatidylinositol-specific phospholipase C. 135 82


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