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 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.
Mol Immunol 1986 Apr
PMID:Solubilization and characterization of a low-affinity histamine-binding site on human blood mononuclear cells. 308 33

The co-operative response of regulated actomyosin ATPase to increasing concentrations of calcium has been attributed to nearest-neighbor interactions, presumably between troponin-tropomyosin complexes. The degree of co-operativity was not decreased after the carboxy-terminal 11 amino acid residues had been removed from tropomyosin by carboxypeptidase A. This indicates that the interactions between neighboring troponin-tropomyosin complexes do not occur through the overlapping tropomyosin ends.
J Mol Biol 1985 Mar 20
PMID:Removal of tropomyosin overlap and the co-operative response to increasing calcium concentrations of the acto-subfragment-1 ATPase. 315 45

Chronic urticaria is a changeable disorder with an unknown length of duration. Thus, an objective method which could differentiate affected individuals from healthy individuals and with predictive information about when treatment might be diminished or stopped would be desirable. Therefore, we have tried to achieve this by means of Multitest, a device rendering good skin reaction reproduction and reagents such as 48/80 Compound (a nonspecific mast cell degranulator) and histamine. These substances were applied on 1 to 10(3) Mol concentrations for histamine and 10 to 10(3) mg/ml as the degranulating agent. Sixteen patients and 10 controls were submitted to this test, variables such as drugs modifying wheals, time of the day, age range and skin area were controlled. In both groups a clear dose-response relationship was demonstrated by either reagent. However, an excessive individual variability appeared in each sample and significant differences could not be shown so much for sensitivity or for reactivity (responses by the lowest and the highest concentrations, respectively). We conclude that the lack of differences observed on cutaneous mast cell "releasability" and skin vessels response to histamine in chronic urticaria patients could be due to a rather outstanding role of other cells and its mediators, in mechanisms of that chronic disease.
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PMID:Skin reactions to histamine and compound 48/80 in chronic urticaria: a diagnostic tool? 338 11

We have examined genomic sequences and mRNA species hybridizing to a cDNA clone of a yolk sac carcinoma chondroitin sulfate proteoglycan designated PG19. Genomic blot hybridizations with cDNAs covering the majority of the PG19 mRNA sequence revealed 15 to 17 gene fragments. Similar analysis with probes representing either the propeptide or the combined core protein COOH-terminal domain and 3' untranslated sequences revealed single genomic fragments indicating that a single gene codes for the PG19 proteoglycan. Genomic blot analysis with cDNA sequences coding for the serine-glycine repeat of the core protein identified the same gene fragments observed with the entire PG19 cDNA, indicating that this coding region is homologous with sequences present in multiple genes. The same probes were also used to examine mRNA expression. In addition to the PG19 mRNA, several PG19-related mRNAs could be seen. These PG19-related mRNAs had homology with the serine-glycine coding sequence of the PG19 cDNA. These mRNAs may be coding for proteoglycans. The mRNA coding for PG19 appeared to be uniquely expressed in parietal yolk sac and mast cell lineages. The PG19 mRNA existed in different forms in parietal yolk sac and mast cell lines due to cell-type-specific differences in the length of the 5' untranslated sequences. These results indicate that expression of the PG19 proteoglycan gene is regulated both in terms of cell-type-specific transcription and selection of a transcriptional start site.
Mol Cell Biol 1987 Jan
PMID:Gene expression of the chondroitin sulfate proteoglycan core protein PG19. 356 92

The structural difference between two forms (basic and acidic) of guinea-pig beta 2-microglobulin (beta 2m) has been established. Both forms are present in urine from inbred guinea-pig strains. The beta 2m forms were each digested with carboxypeptidase Y and carboxypeptidase A contaminated with carboxypeptidase B. Released amino acids were separated from remaining protein, dansylated and analysed by 2-dimensional TLC on polyamide layer sheets. From the results it was concluded that the basic beta 2m form has lysine and the acidic beta 2m form has asparagine as their respective C-terminal amino acids. The acidic form is also 1 amino acid (lysine) shorter than the basic form, which is supported by electrophoretic studies on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The presence of the 2 forms of beta 2m in urine from inbred guinea-pig strains 2 and 13, shown by gel filtration and ion exchange chromatography, makes it unlikely that the 2 forms are a result of genetic polymorphism.
Mol Immunol 1985 Sep
PMID:Structural difference between the two forms of guinea-pig beta 2-microglobulin and their occurrence in inbred guinea-pig strains. 393 25

As demonstrated by labeling with peroxidase, avidin was found to bind selectively and distinctly to mast cell granules. Inhibition studies suggested that avidin is bound by heparin. Based on this new mast cell staining procedure, mast cell distribution in the inflamed synovium of rheumatoid arthritis (RA) and osteoarthritis (OA) has been investigated. In the subsynovial layer, a significant decrease in mast cell numbers was observed in RA-synovium when compared with OA-synovium. This decrease correlated with the presence of lining cell ulcers and granulation tissue and can be interpreted as the result of mast cell degranuation induced by complement-mediated or immune complex-triggered mechanisms.
Virchows Arch B Cell Pathol Incl Mol Pathol 1984
PMID:Analysis of mast cells in rheumatoid arthritis and osteoarthritis by an avidin-peroxidase staining. 608 57

Cytophilic antibodies of the IgE class play two distinctive roles in the immunological triggering of mast cell, initially by binding to Fc receptors on the plasma membrane and secondly, by transmitting to the sensitised target cell the effects of their subsequent interaction with specific antigen (allergen). In contrast to the claim that the IgE antibody merely acts as a surrogate receptor in its latter role, evidence is presented in support of the contention that it is actively involved in mast cell triggering by providing a signal to a second "receptor" [i.e. other than Fc(epsilon)R]. Synthetic peptide studies have provided an insight into the structural characteristics of such an Fc effector site, besides beginning to suggest the manner of its interaction with the mast cell membrane. In discussing the implication of our findings, this type of immunological trigger process is contrasted with that brought about by hormone agonists. It is suggested that the cytophilic IgE antibody can be regarded as a pro-hormone, which only gains hormonal status as a result of cross-linking by specific antigen.
Mol Immunol 1984 Dec
PMID:The role of non-antigen receptors in mast cell signalling processes. 608 73

Human skeletal muscle acylphosphatase, purified by a technique based on affinity chromatography on immunoadsorbent, has been sequenced completely using tryptic and peptic peptide series, prepared by reverse-phase high-pressure liquid chromatography. The sequence analysis was carried out on all the isolated tryptic peptides using a manual Edman degradation technique and time-course analysis of the released amino acids by carboxypeptidase A. The enzyme is NH2-blocked and the blocking group has been identified by fast atom bombardment mass spectrometry.
Mol Biol Med 1984 Dec
PMID:Human skeletal muscle acylphosphatase: the primary structure. 610 Jul 23

The tissue mast cell is the major storage site of histamine in the body. The present study is concerned with the effect of one histamine H1- and one histamine H2-receptor antagonist on proliferation in the rat mesentery following drug-induced mast-cell secretion. The H2-receptor antagonist, but not the H1-receptor antagonist, significantly suppressed mast-cell-mediated proliferation in vivo and in organ-cultured mesentery. This finding indicates that mast-cell-histamine is a mitogen acting directly on histamine H2-receptors in surrounding tissue cells.
Virchows Arch B Cell Pathol Incl Mol Pathol 1980
PMID:Mast cell histamine, a local mitogen acting via H2-receptors in nearby tissue cells. 610 3

Rats with diabetes of 4 weeks' duration have previously demonstrated increased mitogenesis in normal connective tissue cells following mast cell secretion. The appearance of this augmented mast cell-mediated mitogenic reactivity was studied in the mesentery of insulin-deficient rats, 3, 7, and 28 days after they had been rendered diabetic by a single dose of streptozotocin. On day 7 mast cell secretion induced a subnormal mitogenic response which, however, increased above normal on day 28. This time lag in the augmentation of mitogenic responsiveness may be important since proliferative lesions in diverse mesenchymal tissues typically develop with a similar delay in both experimental and clinical diabetes.
Virchows Arch B Cell Pathol Incl Mol Pathol 1982
PMID:Delayed mast cell mediated mitogenic reactivity in diabetic rats. 613 82


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