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)

This paper reports that the ionophore-induced slow-reacting substance (SRS) from mast cell tumor leukocytes is a member of a group of compounds called leukotrienes. Briefly, murine mastocytoma cells treated with calcium ionophore produced a SRS that caused guinea pig ileum to contract. This response could be reversed by an SRS antagonist, FPL 55712. Based on osotope incorporation experiments, spectrophotometry, and chemical degradation analyses, the SRS was identified. It is a cysteine-containing derivative of 5-hydroxy-7,9,11,14-icosatetraenoic acid, which was attached in a thioether linkage at C-6. The SRS was structurally related to previously identified epoxy and dihydroxy metabolites of arachidonic acid in leukocytes. The leukotrienes have the common feature of the presence of a conjugated triene. Leukotriene A is an intermediate in the formation of leukotriene B, and is proposed to be the precursor also of leukotriene C, the SRS chemically identified in this paper.
Proc Natl Acad Sci U S A 1979 Sep
PMID:Leukotriene C: a slow-reacting substance from murine mastocytoma cells. 4 Dec 40

Changes in rat mast cell cyclic adenosine 3',5' monophosphate (cAMP) concentrations during stimulation of histamine release by concanavalin A (con A) and anti-IgE were studied. Con A caused an increase in cAMP with a mean peak level at 20 sec of 232% of control (range 164% to 365%). Con A-stimulated cells demonstrated falls toward control levels after 20 sec, but generally remained above control for at least 5 min. By 10 min cAMP had returned to control values. The con A effect on cAMP occurred in the absence of phosphatidyl serine but was markedly inhibited by 5 mM alpha-methyl-D-mannose. Anti-IgE induced a less marked increase in cAMP (157% of control, range 110% to 540% of control) which reached a peak at 20 sec. Two monospecific goat anti-rat myeloma IgE antisera induced similar changes in cAMP whereas normal goat IgG had no effect. These peak values were followed by a rapid decrease in cAMP. Within 2 min the cAMP content of anti-IgE stimulated cells had fallen to levels well below control and remained below control levels from 45 sec to over 15 min. Histamine release in both systems began after the peak cAMP levels, during the period of rapid destruction of cAMP.
J Immunol 1976 Sep
PMID:Modulation of cyclic AMP in purified rat mast cells. III. Studies on the effects of concanavalin A and anti-IgE on cyclic AMP concentrations during histamine release. 6 Apr 47

The mast cell in tissues represents an effector cell capable of elaboration of all the essential mediators of inflammation. The effects of uncontrolled activation may be divided into pharmacologic and inflammatory phases with attendant implications for the initiation of both acute and subacute pathologic processes. The elaboration of chemical mediators by the mast cell makes it possible to recruit blood cells and proteins essential to host defense by a controlled physiologic process that can proceed without significant local tissue damage. When uncontrolled, the same potentiality can be injurious, with the nature of the clinical problem depending upon the location of the cells, the intensity of activation, and the ratio of newly generated and preformed mediators released. The evidence that the mast cell can participate in each form of immunologic reaction--immediate, immune complex, and delayed- as a primary or secondary effector cell and the diversity of its products foretell an evolving recognition of its role in host defense and tissue injury. It is pertinent to develop further methods and criteria to define the nature and extent of mast cell participation in disease processes.
J Invest Dermatol 1976 Sep
PMID:The diversity of mast cell-derived mediators: implications for acute, subacute, and chronic cutaneous inflammatory disorders. 6 Dec 46

Changes in the surface morphology of secreting mast cells have been followed by scanning electron microscopy. Mast cells isolated from the rat peritoneal cavity have folds of plasma membrane that form snake-like ridges on their surfaces. Fold length varies considerably from cell to cell, whereas fold width and depth appear to remain relatively constant. To assess the possible relationship between secretory activity and surface folding, a seimquantitative method was used for measuring fold length in control and secreting populations. A positive correlation is found between secretion of histamine and the extent of membrane folds on the mast cell surface. The source of the membrane required for fold formation is probably secretory granule membrane incorporated into the plasma membranene as a result of exocytosis. Furthermore, a distinct cell type devoid of surface folds, designated as a raspberry-type cell, is found to occur as an integral part of a normal population of mast cells. This cell type is resistant to stimulation by polymyxin.
J Cell Biol 1977 Sep
PMID:Plasma membrane folds on the mast cell surface and their relationship to secretory activity. 7

Microspectrophotometric analyses combined with model experiments using polyacrylamide films containing different types of purified glycosaminoglycan or glycosaminoglycan and basic protein, have been applied to investigate the chemical characteristics of the glycosaminoglycan moiety present in rat mucosal mast cell granules. The results obtained with these histochemical techniques present evidence of the absence of significant amounts of heparin and the presence of lower sulfated glycosaminoglycan(s) in the granules of these cells.
J Histochem Cytochem 1977 Sep
PMID:Does heparin occur in mucosal mast cells of the rat small intestine? 7 26

Twenty-three dogs completed a fractionated course of ionizing radiation therapy for mast cell tumors. In 10 dogs the response was satisfactory, and the tumors were considered controlled 12 months after completion of the prescribed course of therapy. Treatment was considered unsatisfactory for the remaining 13 dogs due to failure to control the tumor locally, generalized metastasis, or both. A dose effect was noted in the response of the tumors to radiation. Of 6 dogs, 5 responded satisfactorily when the tumor dose was 4,000 rads or greater. When the tumor dose was less than 4,000 rads, 5 of 17 dogs responded satisfactorily. The dose calculated to control 50% of the meat cell tumors was 3,625 rads (95% confidence interval: 3,265-4,024 rads). Adverse normal tissue reactions, which consisted of moist desquamation in 10 animals and necrosis in 4, were recorded. The dose calculated to cause desquamation in 50% of the dogs was 3,750 rads (95% confidence interval: 3,348-4,200 rads).
J Natl Cancer Inst 1979 Sep
PMID:Response of canine mast cell tumors to radiation. 11 13

Angiotensin-converting enzyme has been solubilized from a particulate fraction of rabbit lung and purified to apparent homogeneity in 11% yield by a procedure including fractionation with DEAE-cellulose and calcium phosphate gel, elution from Sephadex G-200, and lectin affinity chromatography. The molecular weight estimated by equilibrium sedimentation was approximately 129,000, either in the absence or presence of 6 M guanidine hydrochloride. A slightly higher value of 140,000 determined for the reduced, denatured protein by gel electrophoresis in the presence of sodium dodecyl sulfate and a much higher figure derived from gel filtration are probably due to the glycoprotein nature of the enzyme. Its oligosaccharide content accounted for 26% of the weight calculated from its amino acid and carbohydrate composition. The estimated content of sugar residues per mole was: galactose, 57; N-acetylglucosamine, 53; mannose, 43; N-acetylneuraminic acid, 19; and fucose, 4. Threonine and alanine were identified, respectively, as NH2-terminal and COOH-terminal residues by the dansylation procedure and by digestion with carboxypeptidase A. The enzyme was found to contain approximately 1 g atom of zinc per mol. Km values for hydrolysis of hippurylhistidylleucine and angiotensin I were 2.3 and 0.07 mM, and the corresponding turnover numbers were 15,430 and 792 mol/min/mol at 37 degrees. Bradykinin was also a substrate, and release of its COOH-terminal dipeptide, Phe-Arg, was catalyzed at a comparable rate to that of His-Leu from the COOH terminus of angiotensin I. Enzyme activity required the presence of chloride ions and was inhibited by EDTA and by low concentrations of Bothrops bradykinin-potentiating peptides. In addition, hydrolysis of hippurylhistidylleucine was inhibited competitively by other defined peptides, including di- and tripeptides, which were not substrates.
J Biol Chem 1975 Sep 10
PMID:Pulmonary angiotensin-converting enzyme. Structural and catalytic properties. 16 57

Glucagon1-21 has been prepared by treating native glucagon with carboxypeptidase A. Purified glucagon1-21 did not contain detectable methionine (less than 0.001 residue/mol) and the activity of the compound did not change after treatment with cyanogen bromide as has been shown with native glucagon. Glucagon1-21 stimulates hepatic adenylate cyclase activity to the same extent as native glucagon but with 0.1% the potency. Glucagon1-21 also displayed 0.1% the binding affinity of native glucagon to the glucagon receptor in hepatic membranes. Glucagon22-29 alone or in combination with glucagon1-21 did not activate adenylate cyclase or displase 125I-glucagon from its receptor. The finding that glucagon1-21 is a full agonist on adenylate cyclase is discussed in relation to the structure-function relationships required for the biological action of glucagon.
J Biol Chem 1978 Sep 25
PMID:A reassessment of structure-function relationships in glucagon. Glucagon1-21 is a full agonist. 21 Jan 80

To investigate mechanisms of mast-cell proliferation, we have utilized infection of Lewis rats with the intestinal nematode, Nippostrongylus brasiliensis, which induces a pronounced intestinal mast-cell hyperplasia. Adoptive transfer of 2 x 10(8) immune mesenteric lymph node cells (IMLN), collected 14 days post infection with 3000 third stage larvae (L3), into rats concurrently given 3000 L3 hastened the expected intestinal mastocytosis by up to 4-5 days. IMLN exhibited this mastopoietic activity in the presence but not in the absence of concurrent infection. Normal mesenteric lymph node cells did not show similar mastopoietic activity. Intestinal mastocytosis was delayed by sub-lethal irradiation (400 rad) but IMLN reconstituted the mast-cell response of such animals. The mastopoietic activity could not be attributed to worm antigen as antigen administered intravenously had no significant effect on mastocytosis and furthermore, antigen could not be detected in mastopoietically active IMLN suspensions used as a possible antigen source in passive cutaneous anaphylaxis tests. Immune serum (14 days post primary infection with 3000 L3) also hastened mastocytosis in infected rats, whereas normal serum did not. The IMLN may be an enriched source of intestinal mast cell precursors and, in addition, may contain a cell type(s) which regulates the differentiation and proliferation of such precursors.
Immunology 1979 Sep
PMID:Immunologically mediated intestinal mastocytosis in Nippostrongylus brasiliensis-infected rats. 31 19

1. Isolated rat peritoneal mast cells incubated in Ca-free media for 2 h, with or without EDTA, and observed by phase-contact microscopy, became ;bubbled' in appearance when subsequently exposed to media rich in calcium (16-110 mM).2. Electron microscopy showed the response to be ;compound' exocytosis of the sort elicited by conventional mast cell secretagogues such as antigen (in sensitized cells) and 48/80.3. The response to Ca was inhibited by withdrawing glucose and adding dinitrophenol and was thus energy-dependent.4. Mg in similarly high concentration had no such stimulant effect on Ca-deprived cells, and excess Ca stimulated only after Ca deprivation.5. It is suggested that Ca deprivation may increase the permeability of the plasma membrane of the mast cell thereby allowing some Ca, when subsequently introduced in high concentration, to penetrate and activate exocytosis; and the results are considered further support for the postulated mediator function of Ca in stimulus-secretion coupling.6. Two inhibitory effects of calcium in high concentration were detected: (a) suppression of migration or expulsion of granules from the exocytotic pits within the cellular domain; and (b) diminished sensitivity to 48/80.
J Physiol 1977 Sep
PMID:Calcium and stimulus-secretion coupling in the mast cell: stimulant and inhibitory effects of calcium-rich media on exocytosis. 33 97


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