Maurice B. Feinstein

TL;DR: The hypothesis that inositol 1,4,5-trisphosphate is a second messenger mediating the release of Ca2+ from intracellular storage sites is supported.

TL;DR: The ability of phorbol 12-myristate 13-acetate to initiate neutrophil responses similar to those produced by the chemotactic factor without causing a rise in the level of intracellular free calcium suggests two possibilities; that there is a second messenger in addition to calcium or that it activates the cells at a point distal to calcium mobilization.

TL;DR: In this article, it is suggested that cAMP-dependent reactions maintain low levels of cytoplasmic Ca2+ by promoting transport and binding of Ca2+, which coincides with the reversal of thrombin-induced, Ca2-dependent protein phosphorylation, and cytoskeleton assembly.

TL;DR: Antagonism of calmodulin provides a molecular mechanism that may explain the inhibition of many Ca2-dependent cellular processes by local anesthetics--e.g., Ca2+ transport, exocytosis, excitation-contraction coupling, non-muscle-cell motility, and aggregation.

TL;DR: Results suggest that activation of protein kinase C, which initially fosters secretion and aggregation, may subsequently exert negative feedback on the receptor-mediated mobilization of intracellular Ca2+ and the hydrolysis of phosphatidylinositol 4,5-bisphosphate.