jasplakinolide has been researched along with 2-tert-butylhydroquinone* in 1 studies
1 other study(ies) available for jasplakinolide and 2-tert-butylhydroquinone
Article | Year |
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Two pathways for store-mediated calcium entry differentially dependent on the actin cytoskeleton in human platelets.
A major pathway for stimulated Ca(2+) entry in non-excitable cells is activated following depletion of intracellular Ca(2+) stores. Secretion-like coupling between elements in the plasma membrane (PM) and Ca(2+) stores has been proposed as the most likely mechanism to activate this store-mediated Ca(2+) entry (SMCE) in several cell types. Here we identify two mechanisms for SMCE in human platelets activated by depletion of two independent Ca(2+) pools, which are differentially modulated by the actin cytoskeleton. Ca(2+) entry induced by depletion of a 2,5-di-(tert-butyl)-1,4-hydroquinone (TBHQ)-sensitive pool is increased by disassembly of the actin cytoskeleton and that induced by a TBHQ-insensitive pool is reduced. Stabilization of the actin cytoskeleton prevented Ca(2+) entry by both mechanisms. We propose that the membrane-associated actin network prevents constitutive Ca(2+) entry via both pathways. Reorganization of the actin cytoskeleton permits the activation of Ca(2+) entry via both mechanisms, but only SMCE activated by the TBHQ-insensitive pool requires new actin polymerization, which may support membrane trafficking toward the PM. Topics: Actins; Animals; Antineoplastic Agents; Biological Transport; Blood Platelets; Bridged Bicyclo Compounds, Heterocyclic; Calcium; Calcium-Transporting ATPases; Cytochalasin D; Cytoskeleton; Depsipeptides; Enzyme Inhibitors; Humans; Hydroquinones; Nucleic Acid Synthesis Inhibitors; Peptides, Cyclic; ras Proteins; Signal Transduction; Thiazoles; Thiazolidines | 2004 |