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 effects of TMB-8 and calmidazolium were investigated on mast cell responses believed to be mediated by protein kinase C, i.e. histamine release induced by TPA (tetradecanoyl-phorbol-acetate) in combination with sub-threshold concentrations of the ionophore A23187 and with antigen. Inhibition with both drugs was found in the same concentration range as observed earlier and could be counteracted by glucose, indicating an impaired oxidative energy production. Hence, the test drugs do not reveal protein kinase C selectivity.
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PMID:Influence of TMB-8 and calmidazolium on phorbol ester promoted histamine release from isolated rat mast cells. 169 33

Changes in intracellular calcium levels induced in mast cells by either antigen or ionomycin were monitored using flow cytometry and the calcium binding dye indo-1. Both stimuli increased calcium levels in responsive cells by a similar amount, but not all cells examined were responsive to antigen. Antigen-induced increases in intracellular calcium levels could be completely blocked by the calcium antagonist TMB-8. Flow cytometry appears to be a useful method for monitoring mast cell calcium concentrations, as it provides the capability to study large numbers of individual cells.
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PMID:Calcium mobilization in activated mast cells monitored by flow cytometric analysis. 208 41

The effects of Con A on free cytoplasmic calcium concentrations in the cloned murine mast cell, MC9, have been measured using the fluorescent calcium indicator quin 2. Con A causes a rapid, small yet sustained rise in free cytosolic calcium (up to 245 nM) followed closely by increased 45calcium uptake and more slowly by histamine release. The increases in 45calcium uptake and histamine release require extracellular calcium. However, the Ca2+ influx blockers, nifedipine and verapamil inhibit these responses only at concentrations significantly higher than those used in smooth muscle to oppose potential-dependent events, and diltiazem is inactive. These observations suggest that, in these mast cells, other types of channels control Ca2+ entry. In contrast, the intracellular Ca2+ blocker, TMB-8, inhibits both the Con A-induced histamine release and the Ca2+ changes. The calmodulin antagonists calmidazolium, trifluoperazine and W-7 are also highly effective inhibitors of both the Ca2+ changes and histamine release in direct proportion to their potency against calmodulin-dependent phosphodiesterase, implicating calmodulin in the regulation of stimulus-secretion in MC9 cells. These data imply that histamine release follows increases in intracellular Ca2+ concentration. Free intracellular Ca2+ results from rapid release from internal stores and is followed by a slower but more sustained influx of extracellular Ca2+.
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PMID:The role of a Ca2+/calmodulin dependent plasma membrane Ca2+ channel during concanavalin A activation of MC9 mast cells. 244 80

4-Aminopyridine (4-AP), a known potassium channel blocker, was shown to induce histamine release from mast cells in mice. After ip 4-AP 5 mg.kg-1 the histamine content increased in blood, but decreased in the lung tissue. Calcium antagonists nifedipine (NIF) 500 mg.kg-1 ig, TMB-8 300 mumol.L-1 in vitro and potassium channel opener minoxidil (MIN) 100 mg.kg-1 inhibited the histamine release induced by 4-AP from mouse peritoneal mast cells (PMC). These results provide evidence that potassium channels are present in mouse mast cell membranes and indicate that the mechanism of histamine release by 4-AP may be related to the potassium channel blocking effect. As the result of this effect, the calcium channels open and the Ca2+ influx to the mast cells increases, thus eliciting histamine release.
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PMID:[4-Aminopyridine induced histamine release and its antagonism by certain drugs]. 752 60