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

The magnetic circular dichroic (MCD) spectra of cobalt(II) sugstituted metalloenzymes have been studied and compared to a series of four-, five-, and six-coordinate cobalt(II) model complexes previously examined (T. A. Kaden et al. (1974), Inorg. Chem. 13, 2582). The MCD spectra of cobalt substituted carboxypeptidase A, procarboxypeptidase ta, and thermolysin are consistent with earlier deductions of tetrahedral coordination from absorption spectra and also with X-ray structure analysis. Inhibitors fail to alter their MCD spectra significantly. The MCD spectra of cobalt alkaline phosphatase and carbonic anhydrase are more complex and their pH dependence and alteration by inhibitors are discussed in terms of known cobalt(II) models.
 ...
PMID:Magnetic circular dichroic spectra of cobalt(II) substituted metalloenzymes. 23 52

A 68-year-old man presented with a 6-month history of fatigue, rhinorrhoea, pruritic skin lesions, left pleural effusion, ascites, oedema and weight loss of 10 kg. Investigations revealed hepatosplenomegaly, retroperitoneal lymphadenopathy, anaemia, leucocytosis with eosinophilia, hypoprothrombinaemia, hypocholesterolaemia and elevation of both gamma glutamyltransferase and alkaline phosphatase. Biopsies of a skin lesion, bone marrow and liver revealed mast cell infiltration, allowing the diagnosis of systemic mastocytosis (SM). Hydroxyzine plus ranitidine were given without success. Hydroxyzine treatment was stopped, and ketotifen was initiated; substantial symptomatic improvement was observed within 8 d. This case report indicates the effectiveness of ketotifen in the symptomatic treatment of SM.
 ...
PMID:A case of systemic mastocytosis; therapeutic efficacy of ketotifen. 204 Aug 76

A 59-year-old male presented with systemic mastocytosis with extensive skeletal involvement resulting in vertebral compression fractures and bone pain. Histomorphometric analysis of bone revealed increased mast cells, elevated static parameters of bone resorption, and low bone formation. Serum calcium, phosphorus, and alkaline phosphatase were normal; however, serum 1,25-dihydroxyvitamin D3 and osteocalcin levels were low. Histamine levels in plasma and urine were elevated. Following therapy with ketotifen, the patient had resolution of bone pain along with decreased flushing and pruritus. Elevated plasma and urine histamine levels normalized, as did 1,25-dihydroxyvitamin D3 and osteocalcin levels. Indices of low bone formation improved on therapy. Eroded surfaces improved but remained elevated. This case is the first demonstration that bone symptoms and histomorphometric change in systemic mastocytosis are reversed with inhibition of mast cell degranulation. The role of mast cells and their products in bone metabolism is poorly understood, but the therapy of bone disease in systemic mastocytosis should include inhibition of the release of mast cell products along with the use of histamine antagonist.
 ...
PMID:Inhibition of mediator release in systemic mastocytosis is associated with reversal of bone changes. 227 Jul 75

Lesional (n = 15) and non-lesional (n = 10) skin of subjects with mastocytosis was analysed for the distribution and concentration of trypase positive, chymase negative mast cells (MCT) and tryptase positive, chymase positive mast cells (MCTC) cells and compared to normal skin (n = 23) and non-lesional skin of subjects with unexplained anaphylaxis or flushing episodes (n = 6). Skin biopsies were fixed in Carnoy's fluid and subjected to double immunohistochemical staining with biotinylated mouse monoclonal anti-chymase antibody followed by alkaline phosphatase-conjugated mouse monoclonal anti-tryptase antibody. MCTC cells were the only type of mast cells seen in all specimens analysed and in each case were more numerous in superficial compared to deep regions of dermis. The concentration (mean +/- s.d.) of mast cells in the superficial dermis of mastocytosis lesions (40 985 +/- 21 772 mast cells/mm3) was significantly increased over that in corresponding areas of non-lesional skin from subjects with mastocytosis (7178 +/- 3607 mast cells/mm3), skin from subjects with idiopathic anaphylaxis or flushing episodes (6974 +/- 3873 mast cells/mm3) and normal skin (7347 +/- 2973 mast cells/mm3). The exclusive presence of MCTC cells in skin lesions of mastocytosis which are characterized by non-malignant hyperplasia of mast cells suggests involvement of local tissue factors in mast cell recruitment and differentiation.
 ...
PMID:Mast cells in cutaneous mastocytosis: accumulation of the MCTC type. 231 Sep 82

This study identifies the in vitro differences (markers) between virulent and attenuated transmissible gastroenteritis (TGE) viruses. Exposure of virulent Miller strain and attenuated Purdue strain TGE viruses to a spectrum of acidities indicated that the Miller strain was more stable at pH 2. Acidities at or above pH 3 did not reduce viral infectivity of either strain. When virulent and attenuated viruses were exposed to gastric fluids of either fed or fasted swine, there was a similar degree of sensitivity. Carboxypeptidase B, alpha-amylase, and alkaline phosphatase present in porcine small intestinal fluids did not cause a significant difference in sensitivity between virulent and attenuated virus isolates. The digestive enzymes: trypsin, alpha-chymotrypsin, pancreatin, peptidase, and carboxypeptidase A did not (or only slightly) inactivate virulent Miller strain TGE virus, but greatly reduced infectivity of attenuated viruses (Purdue strain and TGE vaccine virus isolates). The attenuated strains were significantly more sensitive to small intestinal fluids from both fasted and fed adult swine. Differential sensitivities between virulent and attenuated TGE viruses to digestive fluids from stomach and small intestine further substantiate the notion of differential susceptibility to small intestinal proteases as a correlate of viral virulence.
 ...
PMID:Enzymatic and acidic sensitivity profiles of selected virulent and attenuated transmissible gastroenteritis viruses of swine. 298 96

Derivatives of D-luciferin, D-luciferin methyl ester, D-luciferin O-sulfate, D-luciferin O-phosphate, D-luciferyl-L-N alpha-arginine and D-luciferyl-L-phenylalanine were used as highly sensitive substrates for carboxylic esterase, arylsulfatase, alkaline phosphatase and carboxypeptidases A, B and N. Enzymatic cleavage of the compounds by enzymes leading to the release of D-luciferin was demonstrated. Kinetic constants have been determined for D-luciferin methyl ester and carboxylic esterase, for D-luciferin O-sulfate and arylsulfatase, for D-luciferin O-phosphate and alkaline phosphatase, for D-luciferyl-L-phenylalanine and carboxypeptidase A, and for carboxypeptidases B and N and D-luciferyl-L-N alpha-arginine. All compounds proved to be highly sensitive substrates for the respective enzymes, permitting a limit of detection for enzymes between 10 and 500 fg per assay.
 ...
PMID:A new type of ultrasensitive bioluminogenic enzyme substrates. I. Enzyme substrates with D-luciferin as leaving group. 316 46

Derivatives of luciferin, D-luciferin methyl ester, D-luciferyl-L-phenylalanine, D-luciferyl-L-N alpha-arginine, D-luciferin-O-sulphate and D-luciferin-O-phosphate, were synthesized for use as highly sensitive substrates for enzyme assays. The luciferin derivatives were characterized by ultraviolet and fluorescence spectrophotometry, by amino acid analysis and by fast atom bombardement mass spectrometry. Enzymatic cleavage of the compounds by enzymes leading to the release of D-luciferin was demonstrated. Kinetic constants were determined for the following enzyme/substrate pairs: D-luciferin methyl ester/carboxylic esterase, D-luciferyl-L-phenylalanine/carboxypeptidase A, D-luciferyl-L-N alpha-arginine/carboxypeptidase B, D-luciferin-O-sulphate/arylsulphatase, D-luciferin-O-phosphate/alkaline phosphatase. All compounds proved to be acceptable substrates for the respective enzymes, D-luciferin-O-phosphate being accompanied by an especially high turnover number (kcat = 1010 s-1) with alkaline phosphatase.
 ...
PMID:Synthesis and characterization of luciferin derivatives for use in bioluminescence enhanced enzyme immunoassays. New ultrasensitive detection systems for enzyme immunoassays, I. 354 62

Mouse bone marrow-derived mast cells passively sensitized with monoclonal IgE released paf-acether (platelet-activating factor) and beta-hexosaminidase when challenged with the specific antigen. The formation and the release of paf-acether followed an early increase in the activity of the acetyltransferase, the main enzyme in paf-acether biosynthesis. The antigen-induced activation of the acetyltransferase was dependent on physiologic temperature and on the presence of Ca2+. By using microsomal fractions from unchallenged and challenged mast cells, the Vmax values were 3.5 and 12.0 nmol/min/mg of protein, respectively, whereas in both cases a Km value for acetyl-coenzyme A of 172 microM was measured. The stimulation of acetyltransferase could be mimicked in vitro under experimental conditions which favor phosphorylation, i.e. adding ATP and Mg2+ to lysates from unchallenged mast cells. In contrast, ATP and Mg2+ were uneffective on lysates from challenged cells that exhibited high level of acetyltransferase activity, suggesting that phosphorylation of the enzyme already took place at the time of cell stimulation. Moreover, addition of alkaline phosphatase to microsomal fraction obtained from either antigen-challenged mouse bone marrow-derived mast cells or unchallenged cells, resulted in 52% and 43% loss of acetyltransferase activity, respectively. Phorbol myristate acetate treatment of cells doubled the enzyme activity supporting the phosphorylation hypothesis. Thus, we report on the immunologic activation of a key enzyme for paf-acether synthesis and on the mechanism of this activation in a pure mast cell population. A link between bridging of IgE receptors and the activation of an enzyme critical to the formation of a lipid mediator is thereby evidenced.
 ...
PMID:Biosynthesis of paf-acether. IX. Role for a phosphorylation-dependent activation of acetyltransferase in antigen-stimulated mouse mast cells. 358 83

Thirteen patients with systemic mast cell disease were studied in order to define the hepatic changes in this disease and to correlate the histologic lesions in the liver with the clinical findings. These patients often presented with multisystem disorders and 10 had hepatomegaly. Microscopically, the liver tissues in all patients showed fibrosis and chronic inflammatory cellular infiltration with plasma cells, lymphocytes, eosinophils, and mononuclear fibroblast-like cells in the portal area. The hepatic sinusoids were not significantly involved. A histologic diagnosis of systemic mast cell disease is seldom entertained in liver biopsy specimens embedded in paraffin and stained with hematoxylineosin, but can be facilitated in biopsy specimens embedded in plastic such as methacrylate. Tissue mast cells in the cellular infiltrate can be demonstrated best by special staining techniques with Giemsa, toluidine blue, and chloroacetate esterase. The severity of the histologic changes in the liver does not correlate well with the size of the liver or biochemical changes in the blood. Abnormal serum biochemical values were noted primarily in those with dehydration caused by diarrhea and vomiting, and in those with malnutrition. Hepatic function test results were usually normal, except for alkaline phosphatase level, which was elevated in all 13 patients. Although the clinical significance of hepatic involvement in systemic mast cell disease cannot be established with certainty in this study, it is believed that the prognosis of systemic mast cell disease is most intricately related to the systemic effects of mast cell involvement in many other organs, and not to hepatic involvement per se.
 ...
PMID:Hepatic involvement in systemic mast cell disease. 370 70

Liver cirrhosis was induced by consecutive CCl4-treatment of rats (0.5 ml/kg, s.c., 2 times/week) to investigate the effect of TRQ on the acceleration of fibrosis in the liver. An increase of hydroxyproline content in the liver of rats began 12 weeks after the CCl4 treatment and a 1.9-fold increase was observed at week 14 compared with non-CCl4 treated rats. Histamine in the liver increased about 2 times at week 14. Increased numbers of mast cells were seen in the area of proliferated collagen fiber in the liver under microscopic observation, and also a good correlation was recognized between the number of mast cells and the progression of fibrosis. An administration of TRQ to the rats for 2 weeks from week 13 resulted in significant suppression of both the increase in hydroxyproline and histamine in the liver dose-dependently compared with the CCl4 control group. Both progression of collagen and increase in mast cell numbers were also suppressed by TRQ dose-dependently under histopathological observation; at the same time the decrease in mast cells was recognized to correspond to the decrease in hydroxyproline and histamine in the liver. Thus, it was suggested that increased mast cells participated in the biosynthesis of collagen. Though the elevated serum transaminases, alkaline phosphatase and leucine amino peptidase were also suppressed by TRQ administration, the protein biosynthesis activity of the liver and lowered serum total cholesterol were not improved as much as the other parameters. From these results, it was shown that TRQ was especially and remarkably effective in suppressing the acceleration of fibrosis, and one of the pharmacological mechanisms of this action may be ascribed to the inhibitory effect of TRQ on the activation of mast cells by some stimulants.
 ...
PMID:[Suppressive effect of tritoqualine (TRQ) on the acceleration of fibrosis in the liver]. 371 Mar 12


1 2 3 Next >>