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Query: UNIPROT:P15088 (mast cell)
14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The test of indirect degranulation of rat mast cells was applied to the study of the specific activity of 16 series of noninfectious allergens from domestic dust (3 series) from hotel dust (7 series) and from the pollen of fescue (6 series). The concentration of protein nitrogen in the allergens from the domestic and hotel dust constituted to 10 000 PNU, and in the allergen from the pollen of fescue--125 000, 50 000, 15 000 and 7 000 PNU. In studying the specific activity of domestic allergens use was made of the sera of patients suffering from bronchial asthma with a marked allergy to domestic dust sera of patients with pollinoses with a marked allergy to fescue pollen was applied to the study of the specific activity of pollen allergen. For the assessment of the indirect degranulation test in mast cells of rats an index of mast cell degranulation of rats (IMCDR) was employed. It was shown that the IMCDR values were equal to 0.46, 0.58, 0.62 in using the domestic dust and in the case of the hotel dust - from 0.17 to 0.28. The mean values for the group of preparations from the domestic dust were 2.5 times greater than for the group of preparations for the hotel dust and were 0.55 and 0.22, respectively. For the allergen from the fescue pollen the IMCDR values varied from 1.23 to 0.16, and increased with the rise of the protein nitrogen concentration (PNU). Additional studies demonstrated that the specific activity of the domestic dust allergen with the crude sera and with those preserved in frozen condition for 3 to 6 months was almost the same. The results obtained permit to draw a conclusion that the method of indirect degranulation of rat mast cells with trizing of commercial batches of infectious allergens.
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PMID:[Use of the indirect rat mast cell degranulation reaction in vitro for characterization of the specific activity of non-infectious allergens]. 6 80

Cetylpyridinium chloride (CPC) and cetyltrimethylammonium bromide (CETAB) are bound to polyanionic substances by ionic bonds between the positively charged nitrogen of the quaternary salts and the negative groups of polyanions. The mast cell granules and some other structures treated with CPC or CETAB react selectively with acid dyes and fluorochromes. In ultrathin sections treated with CPC, phosphotungstic acid (PTA) greatly enhances the electron density of the granules of mast cells. The possible mechanism of acid dye and PTA binding by CPC or CETAB treated tissues is discussed.
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PMID:Demonstration of mast cell granules by the cetylpyridinium chloride-acid dye (CPC-AD) and cetylpyridinium chloride-phosphotungstic acid (CPC-PTA) methods. 7 37

The crystal structure of penicillopepsin, an extracellular acid protease isolated from the mold Penicillium janthinellum, has been determined at 2.8 A resolution by the method of multiple isomorphous replacement. The resulting electron density map computed from the native structure factor amplitudes and MIR phases has an overall mean figure of merit of 0.90. The molecule is decidedly nonspherical, with the majority of residues in beta-structure. There is an 18-stranded mixed beta-sheet which forms the structural core in the region of the active site. This site, identified by the covalent binding of two EPNP molecules to Asp-32 and Asp-215, is located in a deep groove which divides the molecule into two approximately equal lobes. Both aspartic acid residues in the active site are in intimate contact with one another and the carboxyl group of Asp-32 makes two other important hydrogen-bonded contacts: one with Ser-35 and the other with the main chain peptide bond between Thr-216 and Gly-217. A proposed mechanism for acid protease catalysis is similar in many aspects to that proposed for carboxypeptidase A. The electrophilic component which polarizes the substrate carbonyl bond in the acid proteases is the proton shared between the beta-carboxyl groups of Asp-32 and Asp-215. The beta-carboxyl group of Asp-32 removes a proton from a water molecule bound between this side chain and the substrate; the resultant OH- attacks the carbonyl carbon atom of the substrate molecule. The phenolic -OH group of Tyr-75 donates its proton to the amide nitrogen of the scissile bond of the substrate.
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PMID:Penicillopepsin: 2.8 A structure, active site conformation and mechanistic implications. 33 94

An attempt was made to reduce or eliminate lung mast cells in order to determine the involvement of mast cells in hypoxic pulmonary vasoconstriction. Anesthetized cats were exposed to acute hypoxia (10% O2) 20-24 h after no pretreatment, after total lung irradiation (3,000 r), after intravenous nitrogen mustard, or after combined lung irradiation and nitrogen mustard. None of the treatments reduced total or perivascular lung mast cell density, or reduced the pulmonary vasoconstrictor response to hypoxia. However, an inverse relationship between lung mast cell density and the pulmonary pressor response to hypoxia was observed. These results suggest that the presence of more lung mast cells may oppose hypoxic pulmonary vasoconstriction.
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PMID:Lung mast cells and hypoxic pulmonary vasoconstriction in cats. 62 23

The use of honeybee venoms and their components may assist in the elucidation of the pathophysiology of reactions to honeybee stings. This initial study compared venoms from various sources by chemical and biological assays, and significant variations were observed. Ten different bee venoms were compared by nitrogen analysis, mouse toxicity, hyaluronidase content, and antigenicity. Based on mouse toxicity, hyaluronidase content, and gel diffusion analysis, two groups of bee venoms could be differentiated. Venoms in one group, Group A, were more toxic, contained hyaluronidase, and showed an additional precipitin band. All venoms contained mellitin as a major fraction, which formed nonimmune precipitin bands during gel diffusion analysis. Gel filtration chromatography and dialysis separated the venoms into components that were then identified by enzyme assays, rat mast cell degranulation, hemolytic activity, and gel diffusion analysis. The venoms within Group A showed similar components, some of which, most noticeably hyaluronidase, were not present in Group B. Dialysis showed that a large portion of the venom could pass through a cellophane membrane including a portion of the phospholipase A. Heterogeneous molecular weights were found for phospholipase A by both gel filtration and dialysis, and may reflect variation in carbohydrate content. It appears that bee venom variability for whatever reason, a heterogeneous MW antigen, and a non-immune precipitable component require careful consideration in any study involving this venomm. These studies have yielded relatively pure, identified bee venom components which can be employed in further studies investigating reactions to honeybee stings.
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PMID:Comparison of honeybee venoms and their components from various sources. 80

A proposed mechanism for the catalytic hydrolysis of peptide bonds by acid proteases is similar in many respects to the Zn-carbonyl mechanism previously derived for carboxypeptidase A. In the acid proteases the electrophilic component is the proton shared by Asp-32 and Asp-215; Tyr-75 donates its proton to the amide nitrogen of the scissile bond and an OH- ion from a water molecule bound between the carboxyl group of Asp-32 and the substrate attacks the carbonyl carbon atom.
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PMID:Mechanism of acid protease catalysis based on the crystal structure of penicillopepsin. 89 39

To clarify the relationship between air pollution and mast cell response, the effects of sulfuric acid aerosols on histamine release from lung mast cells of guinea pigs were investigated. Guinea pigs were exposed to 0.3, 1.0 and 3.2 mg/m3 sulfuric acid (H2SO4) aerosols or 4 ppm nitrogen dioxide (NO2) for 2 and 4 weeks. After the exposure, lung mast cell suspensions were isolated by collagenase treatment and antigen- or A23187-induced histamine release was measured. Antigen-induced histamine release from mast cells was significantly enhanced by the exposure to 1.0 and 3.2 mg/m3 H2SO4 for 2 weeks, but exposure to H2SO4 for 4 weeks did not show the enhancement of antigen-induced histamine release. A23187-induced histamine release was significantly enhanced by the exposure to 1.0 mg/m3 H2SO4 or 4 ppm NO2 for 2 weeks, but suppression of histamine release from lung mast cells stimulated with A23187 was observed by the exposure to 3.2 mg/m3 H2SO4 for 4 weeks. The exposure to 0.3 mg/m3 H2SO4 showed no changes in antigen- and A23187-induced histamine release. The combination of 1.0 mg/m3 H2SO4 with 4 ppm NO2 for 2 weeks resulted in no changes in antigen- and A23187-induced histamine release. These results suggested that functional properties of lung mast cells may be altered by a low concentration of H2SO4 aerosol exposure.
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PMID:Enhanced histamine release from lung mast cells of guinea pigs exposed to sulfuric acid aerosols. 137 9

The three-dimensional structure of (L(-)-2-carboxy-3-phenylpropyl) methylsulfodiimine in its complex with the zinc metalloenzyme carboxypeptidase A has been determined at 2.25-A resolution by x-ray crystallographic methods. This is the first example of a sulfodiimine-containing inhibitor binding to a zinc enzyme, and the structure of the enzyme-inhibitor complex reveals that the tetrahedral sulfodiimine group coordinates to the active site zinc ion in unidentate fashion. The zinc-coordinated nitrogen atom of the sulfodiimine group is also within hydrogen bonding distance to active site base Glu-270; presumably, the sulfodiimine is ionized and accepts a hydrogen bond from protonated Glu-270. The other sulfodiimine nitrogen accepts a hydrogen bond from Arg-127, and the inhibitor binds as a possible analogue of the tetrahedral transition state (or intermediate) in a promoted water pathway for peptide hydrolysis. The unidentate sulfodiimine-zinc binding mode observed in this enzyme-inhibitor complex is reminiscent of that observed in sulfonamide complexes with the zinc metalloenzyme carbonic anhydrase II, and the structural features of sulfodiimine- and sulfonamide-zinc interactions exhibit important similarities among recently determined structures of enzyme-inhibitor complexes: ionized nitrogens bind to zinc in each structure, and these nitrogens are engaged in hydrogen bond interactions with neighboring enzyme residues.
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PMID:Structural comparison of sulfodiimine and sulfonamide inhibitors in their complexes with zinc enzymes. 152 41

In mammals, dihydroorotase is part of a trifunctional protein, dihydroorotate synthetase, which catalyzes the first three reactions of de novo pyrimidine biosynthesis. Dihydroorotase catalyzes the formation of a peptide-like bond between the terminal ureido nitrogen and the beta-carboxyl group of N-carbamyl-L-aspartate to yield heterocyclic L-dihydroorotate. A variety of evidence suggests that dihydroorotase may have a catalytic mechanism similar to that of a zinc protease [Christopherson, R. I., & Jones, M. E. (1980) J. Biol. Chem. 255, 3358-3370]. Tight-binding inhibitors of the zinc proteases, carboxypeptidase A, thermolysin, and angiotensin-converting enzyme have been synthesized that combine structural features of the substrates with a thiol or carboxyl group in an appropriate position to coordinate a zinc atom bound at the catalytic site. We have synthesized (4R)-2-oxo-6-thioxohexahydropyrimidine-4-carboxylate (L-6-thiodihydroorotate) and have found that this analogue is a potent competitive inhibitor of dihydroorotase with a dissociation constant (Ki) in the presence of excess Zn2+ ion of 0.17 +/- 0.02 microM at pH 7.4. The potency of inhibition by L-6-thiodihydroorotate in the presence of divalent metal ions decreases in the order Zn2+ greater than Ca2+ greater than Co2+ greater than Mn2+ greater than Ni2+; L-6-thiodihydroorotate alone is less inhibitory and has a Ki of 0.85 +/- 0.14 microM. 6-Thioorotate has a Ki of 82 +/- 8 microM which decreases to 3.8 +/- 1.4 microM in the presence of Zn2+. Zn2+ alone is a moderate inhibitor of dihydroorotase and does not enhance the potency of other inhibitors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mercaptan and dicarboxylate inhibitors of hamster dihydroorotase. 256 32

This study was undertaken to explore the effects of alveolar hypoxia on perivascular and periairway mast cell populations. Pulmonary mast cells were exposed to unilateral alveolar hypoxia by ventilating one lung of a cat with nitrogen. Mast cells from the contralateral lung, which was simultaneously ventilated with air, were used as a control. The granule content of perivascular and airway mast cells was determined from electron micrographs using morphometric methods. In response to alveolar hypoxia there was a 12% (p less than 0.005) decrease in the granule content of perivascular mast cells but no statistically significant change in periairway mast cell content. Perivascular mast cells from the hypoxic lungs did not show any of the morphological changes seen in IgE-mediated mast cell degranulation, such as granule swelling, fusion, or exocytosis. In the hypoxic lung, morphometric analysis revealed a significant decrease in the proportion of heterogeneous-appearing granules in the perivascular mast cells. The different reactivity of perivascular and periairway mast cells may explain why alveolar hypoxia does not induce significant bronchospasm.
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PMID:Effect of alveolar hypoxia on pulmonary mast cells in vivo. 278 45


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