by several cell types, including ECs and tumor cells. The binding of mitogens to their specific receptors triggers intracellular signaling cascades, involving a number of messengers working in a sort of network. In particular, in this review we describe the increases of calcium levels in the cytosol, a

mM KC1, and which gave a substantial signal on lysis with distilled water were used. The [Ca2+]i rose from a resting value of 150\m=+-\56nM(mean \m=+-\SD, n=14) by 127\m=+-\47nMon depolarization with 80mM KC1. Application of T3 (1-100nM) led to an increase (P<0.05) in [Ca2+]i(mean amplitude

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, or intracellular pH had little effect. Mitochondrial poisons produced a small increase in [Ca2+]~, probably due mostly to the effects of severe ATP depletion on the plasma membrane.

Enhanced airway contractility following inflammation by cytokines such as tumor necrosis factor alpha (TNFa) or interleukin-13 (IL-13) involves increased intracellular Ca 2+ ([Ca 2+] i) levels in airway smooth muscle (ASM). In ASM, plasma membrane Ca 2+ fluxes form a key component of [Ca 2+]i

on the surface of Jurkat T cells. Using digital imaging microscopy on live cells, we further show that E3CaG1 binding results in a substantial increase in [Ca2+]i, up to 300 nM. Addition of angiotensin II, a potent vasoconstrictor known to increase [Ca2+]i, also strongly inhibits sGC activity. sGC isolated from

ABSTRACT The relationship between receptor-mediated increases in the intracellular free calcium concentration ([Ca]i) and the stimulation of ion fluxes involved in fluid secretion was examined in the rat parotid acinar cell. Agonist-induced increases in [Call caused the rapid net loss of up to 50

that active Ca uptake by the SR in situ is stimulated by Mg, and that it can affect local MFS [Ca ++] in the presence of a substantial Ca source. These results provide evidence that an increased rate of Ca uptake in 3 mM Mg could account for inhibition of the large force spike associated with Ca-induced Ca

Gillespie algorithm is a stochastically exact algorithm that provides satisfying results in the representation of calcium microdomains. Gillespie’s algorithm can be approximated via the tau-leap method and the chemical Langevin equation (CLE). Both methods lead to a substantial acceleration in computation

Glucose induced bursts of the membrane potential of pancreatic β-cells are at the origin of substantial intracellular calcium increases which, in turn, trig-ger exocytosis of insulin carrying vesicles. In the context of diabetes type II it is aimed to control vesicle exocytosis. This infers