Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The highly sensitive PAP immunoperoxidase method was used to localize the main neutral protease of rat skin. The use of the neutral detergent, Triton X-100, in the reagent and washing solutions was observed to effectively decrease the nonspecific staining. The specific staining was localized to the mast cell granules.
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PMID:The main neutral protease of rat skin is a mast cell enzyme. Immunohistochemical localization of the enzyme in rat skin with the peroxidase-antiperoxidase (PAP) complex method. 11 14

Mangostin (M), a naturally occurring xanthone in the rinds of the fruits of Garcinia mangostana Linn. (Guttiferae) and its derivatives such as 3-0-methyl mangostin (MM), 3,6-di-O-methyl mangostin (DM), 1-isomangostin (IM), mangostin triacetate (MT), mangostin 3,6-di-O-(tetra acetyl) glucoside (MTG) and mangostin-6,6-di-O-glucoside (MOG) were screened for various pharmacological effects in experimental animals. With the exception of DM all the test compounds produced CNS depression characterised by ptosis, sedation, decreased motor activity, potentiation of pentobarbital sleeping time and ether anaesthesia in mice and rats. None of the compounds exhibited analgesic, antipyretic and anticonvulsant effects. With the exception of MOG, none of the test compounds produced significant effects on the cardiovascular system of frogs and dogs. MOG produced myocardial stimulation and a rise in blood pressure which was partially blocked by propranolol. M, IM and MT produced pronounced antiinflammatory activity both by intraperitoneal and oral routes in rats as tested by carrageenininduced hind paw oedema, cotton pellet implantation and granuloma pouch techniques. Antiinflammatory activity for M, IM and MT was observed even in bilaterally adrenalectomised rats. M, IM and MT did not produce any mast cell membrane stabilising effect and the degranulation effect of polymyxin B, diazoxide and Triton X-100 on rat peritoneal mast cells in vitro was not prevented. M, IM and MT did not alter the prothrombin time of albino rats. M alone produced significant antiulcer activity in rats.
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PMID:Pharmacological profile of mangostin and its derivatives. 31 90

Human mast cell heterogeneity was assessed by histochemical and detailed functional criteria using mast cells isolated from foreskin, uterine myometrium and lung parenchyma. The skin mast cells were histochemically distinct from their counterparts in the other two tissues by being predominantly insensitive to blockage of dye-binding following formalin fixation (ca. 80%). Functionally, a wide range of structurally diverse polycationic compounds induced selective histamine release from the skin mast cells (ca. 10% at top concentrations) although these cells were less responsive to immunological ligands and calcium ionophores when compared with the uterine and lung cells. The basic compounds, polyarginine and histone, proved to be more generalised histamine liberators as compared with their structural analogues, polylysine and protamine sulphate, probably by virtue of their high content of arginine residues and hydrophobic nature (histone). Studies with the anaphylatoxin, C3a, and its analogues 21R and C3ades Arg on skin mast cells emphasized the importance of basic amino acids for histamine-liberating peptides. Skin mast cells also proved more susceptible than their uterine counterparts to lysis by the detergents, Triton X-100 and Tween 20, suggesting that fundamental differences in membrane structure and/or fluidity might account for functional heterogeneity within the human mast cell population.
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PMID:Mast cell heterogeneity in man: unique functional properties of skin mast cells in response to a range of polycationic stimuli. 128 7

In mast cells, basophils, and the RBL-2H3 tumor mast cell model, crosslinking cell surface IgE-receptor complexes by multivalent ligands activates a signal transduction pathway that leads to the secretion of histamine, serotonin, and other inflammatory mediators. Receptor crosslinking in RBL-2H3 cells also changes cell surface morphology and increases F-actin assembly. Previously, Robertson et al. demonstrated that crosslinked IgE-receptor complexes become associated with the Triton X-100-insoluble fraction (the "cytoskeleton") of RBL-2H3 cells and raised the possibility that receptor-cytoskeletal association may be a required step in the stimulation of secretion. The studies reported here confirm by flow cytometry that crosslinking cell surface IgE by antigen induces the association of the crosslinked complexes with the detergent-insoluble fraction. Dose-response studies, also reported here, indicate that the detergent insolubility of the complexes does not correlate with secretion. Thus, secretion increases with antigen concentration to a maximum beyond which more antigen causes less, not more, secretion. There is little residual detergent-insoluble IgE at the concentrations of antigen that promote optimal secretion, whereas the association of IgE with the detergent-insoluble fraction is maximal at the high antigen concentrations that result in reduced secretion. The addition of monovalent hapten to reduce the amount of crosslinking caused by high concentrations of antigen increases secretion and simultaneously reduces the association of IgE with the detergent-insoluble fraction. Dihydrocytochalasin B, an inhibitor of antigen-stimulated actin polymerization, also increases the rate and extent of secretion and simultaneously delays the association of crosslinked IgE-receptor complexes with the detergent-insoluble fraction. From these data, we propose that the association of crosslinked IgE receptors with the detergent-insoluble fraction of RBL-2H3 cells increases with increased receptor crosslinking, is enhanced by antigen-induced actin polymerization, and is more likely related to the termination than the stimulation of secretion. The ligand-induced conversion of receptors to a detergent-insoluble form is not restricted to mast cells but occurs in a variety of cell types. Its general function may be to limit the generation or transmission of transmembrane signals.
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PMID:Antigen-dependent transition of IgE to a detergent-insoluble form is associated with reduced IgE receptor-dependent secretion from RBL-2H3 mast cells. 214 64

The potential relationship of an intact membrane organization for the synthesis of chondroitin and chondroitin 4-sulfate was examined after modification of a mouse mast cell microsomal system with the nonionic detergent, Triton X-100. The results indicated that Triton X-100 had no effect on the rate of polymerization but had a slight effect on the size of glycosaminoglycan chains. An "all or nothing" pattern of sulfation of newly formed chondroitin was obtained in both the presence and the absence of Triton X-100, and this pattern did not change whether sulfation was initiated concurrent with or subsequent to polymerization. Sulfation of exogenous [14C]chondroitin and exogenous proteo[3H]chondroitin by the microsomal system required Triton X-100 but still produced an all or nothing pattern rather than a random sulfation pattern. When a 100,000 x g supernatant fraction was utilized for sulfation of [14C]chondroitin or proteo[3H]chondroitin, Triton X-100 was not needed, and a partial sulfation pattern was obtained. However, it was similar to the all or nothing pattern in that it still produced two populations, with some chains nonsulfated and others approximately 50% sulfated. When chondroitin hexasaccharide was used with 3'-phosphoadenylylphospho[35S]sulfate, multiple GalNAc residues of the individual hexasaccharides were found to be sulfated. This was relatively independent of Triton X-100 or the concentration of the hexasaccharide acceptors. With soluble enzyme, sulfation of multiple GalNAc residues on the individual hexasaccharide molecules was even greater, so that trisulfated products were found. These results suggest that efficient sulfation of chondroitin is related to enzyme-substrate interaction more than to membrane organization.
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PMID:Biosynthesis of chondroitin sulfate. Organization of sulfation. 249 90

The extract of human peripheral blood lymphocytes and monocytes treated with Triton X-100, in direct- and competitive-binding studies, with 10(-6)-10(-2) M [14C]histamine contained a low-affinity binding site whose dissociation constant (Kd 1.8 X 10(-4) M) was commensurate with the concns of histamine (10(-6)-10(-3) M) that result from mast cell and basophil degranulation. Binding was enhanced by millimolar concns of divalent cations and by raising the incubation temp from 4 to 37 degrees C. It was inhibited by trypsin, EDTA, agents interacting with thiol groups, and by Triton X-100 concns greater than 0.2%. Thus a low-affinity histamine receptor that maintains its ligand-binding properties after solubilization from the cell surface was identified.
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PMID:Solubilization and characterization of a low-affinity histamine-binding site on human blood mononuclear cells. 308 33

Microsomal preparations from chondroitin 6-sulfate-producing chick embryo epiphyseal cartilage, and from chondroitin 4-sulfate-producing mouse mastocytoma cells, were incubated with UDP-[14C]glucuronic acid and UDP-N-acetylgalactosamine to form non-sulfated proteo[14C]chondroitin. Aliquots of the incubations were then incubated with 3'-phosphoadenylylphosphosulfate (PAPS) in the presence or absence of various detergents. In the absence of detergents, there was good sulfation of this endogenous proteo[14C]chondroitin by the original microsomes from both sources. Detergents, with the exception of Triton X-100, markedly inhibited sulfation in the mast cell system but not in the chick cartilage system. These results indicate that sulfation and polymerization are closely linked on cell membranes and that in some cases this organization can be disrupted by detergents. When aliquots of the original incubation were heat inactivated, and then reincubated with new microsomes from chick cartilage and/or mouse mastocytoma cells plus PAPS, there was no significant sulfation of this exogenous proteo[14C] chondroitin with either system unless Triton X-100 was added. Sulfation of exogenous chondroitin and chondroitin hexasaccharide was compared with sulfation of endogenous and exogenous proteo[14C]chondroitin. Sulfate incorporation into hexasaccharide and chondroitin decreased as their concentrations (based on uronic acid) approached that of the proteo[14C]chondroitin. At the same time, the degree of sulfation in percent of substituted hexosamine increased. However, the degree of sulfation did not reach that of the endogenous proteo[14C]chondroitin. Hexasaccharide and chondroitin sulfation were stimulated by the presence of Triton X-100. However, in contrast to the exogenous proteo[14C]chondroitin, there was some sulfation of hexasaccharide and chondroitin in the absence of this detergent. These results indicate that the intact microsomal system was not accessible to the larger substrates, and that even with detergents exogenous substrates were not sulfated as effectively as newly formed proteo[14C]chondroitin in an intact microsomal system. When the proteo[14C]chondroitin formed by the chick cartilage microsomal system was incubated together with the mast cell microsomal system and PAPS, sulfation only occurred at the 4-position. When the proteo[14C]chondroitin formed by the mouse mast cell microsomal system was incubated together with the chick cartilage microsomal system and PAPS, sulfation only occurred at the 6-position.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Sulfation of chondroitin. Specificity, degree of sulfation, and detergent effects with 4-sulfating and 6-sulfating microsomal systems. 312 87

The effects of zinc acexamate on stress and reserpine ulcers as well as on gastric mast cells degranulation and membrane stability were evaluated in the rat. Zinc acexamate (100 mg/kg) has demonstrated an inhibitory effect on cold-restraint stress and reserpine-induced ulcer in a dose-dependent manner. Pretreatment of rats, prior to cold restraint stress, reduced gastric mast cell degranulation. Zinc acexamate (10(-4) M) inhibits Triton X-100 release of beta-glucuronidase in isolated hepatic lysosomes. These observations suggest that ulcer protective actions of zinc acexamate may be exerted in part through enhancing gastric mucosal resistance by stabilizing biological membrane integrity.
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PMID:Anti-ulcer and membrane stabilizing actions of zinc acexamate. 357 22

Disodium cromoglycate and compounds which elevated levels of cyclic AMP in the mast cell variously inhibited cytotoxic histamine release induced by the surface active agents melittin, Tween 20 and Triton X-100. These results are inconsistent with the postulated effects of the drugs on receptor mediated calcium channels and alternative explanations of their action are considered.
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PMID:Effect of disodium cromoglycate and cyclic AMP-active drugs on cytotoxic histamine release from rat mast cells. 618 90

Interrelationships between the catalytic behavior of glucose-6-phosphatase and the structure of rat-liver microsomal membranes were investigated. 2. Rabbit anti-microsomal serum completely inhibited glucose-6-phosphate hydrolysis in detergent-modified microsomes but showed no inhibitory effect on the enzyme activity of intact or mechanically disrupted vesicles. 2. Controlled proteolysis of intact microsomes using carboxypeptidase A and/or aminopeptidase M largely denatured enzymes situated on the outer surface of the microsomal vesicles such as monodehydroascorbate reductase and cytochrome c reductase. However, it did not affect the glucose-6-phosphatase activity at all, which remained in a latent state within the membrane. 3. Temperature studies on glucose-6-phosphatase have revealed that only the enzyme activity of intact microsomes exhibited a nonlinear Arrhenius plot, whereas detergent-modified microsomes showed a linear temperature response. 4. Treatment of microsomes with phospholipase C and toluene-2,4-diisocyanate resulted in an apparent loss of about 65% and 85% of the original glucose-6-phosphatase activity and was closely correlated with hydrolysis and chemical modification of phosphatidylethanolamine, respectively. These apparent inactivations could be reversed by addition of Triton X-114 alone without any phospholipid supplementation. These observations indicate that glucose-6-phosphatase is buried within the microsomal membrane, not exposed on either side. They also suggest that phospholipids are involved in the glucose-6-phosphate transport mechanism.
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PMID:Investigations on the possible involvement of phospholipids in the glucose-6-phosphate transport system of rat-liver microsomal glucose-6-phosphatase. 624 79


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