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Open AccessJournal ArticleDOI

Elementary and global aspects of calcium signalling.

Michael J. Berridge
- 01 Mar 1997 - 
- Vol. 499, Iss: 2, pp 291-306
TLDR
Using Ca2+ imaging techniques, the opening of individual channels has now been visualized and models have been proposed to explain how these elementary events are coordinated to generate the global Ca 2+ signals that regulate cellular activity.
Abstract
Calcium is a ubiquitous second messenger used to regulate a wide range of cellular processes. This role in signalling has to be conducted against the rigid homeostatic mechanisms that ensure that the resting level of Ca2+ is kept low (i.e. between 20 and 100 nmol l-1) in order to avoid the cytotoxic effects of a prolonged elevation of [Ca2+]. Cells have evolved a sophisticated signalling system based on the generation of brief pulses of Ca2+ which enables this ion to be used as a messenger, thus avoiding its toxic effects. Such Ca2+ spikes usually result from the coordinated release of Ca2+ from internal stores using either inositol 1,4,5-trisphosphate or ryanodine receptors. Using Ca2+ imaging techniques, the opening of individual channels has now been visualized and models have been proposed to explain how these elementary events are coordinated to generate the global Ca2+ signals that regulate cellular activity.

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Citations
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Langevin, population density and moment-based modeling of local and global aspects of intercellular calcium signaling

Xiao Wang
TL;DR: This dissertation presents a Ca2+ release site modeling approach based on a Langevin description of stochastic Ca2-m ediated inactivation of open channels, and shows how Langevin equations in a whole cell model involving a large number of release sites may be replaced by a single Fokker-Planck equation, yielding an extremely compact and efficient local/global whole cell models.
Book ChapterDOI

Control of Mitochondrial Metabolism by Calcium-Dependent Hormones

TL;DR: It is shown that mitochondria are able to integrate oscillating Ca2+ signals into a graded metabolic output and hormone-induced oscillations in [Ca2+]m elicit sustained increases in NADH.
Journal ArticleDOI

Ca2+ signalling system initiated by endoplasmic reticulum stress stimulates PERK activation.

TL;DR: In this article , the authors reveal the existence of a Ca 2+ signal mechanism by which stressor-mediated Ca 2 + release regulates ER stress by tethering a genetically encoded ca 2+ indicator (GCamP6) to the ER membrane.
Journal ArticleDOI

A Tale of two receptors.

TL;DR: In this article, a new model of Ca2+ oscillations in hepatocytes based on these experiments was proposed to investigate the mechanisms controlling P2Y-activated Ca2+, which accounts for Ca2 + regulation of the IP3 receptor (IP3R), the positive feedback from Ca 2+ on phospholipase C (PLC), and the p2Y receptor phosphorylation by protein kinase C(PKC).
References
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Journal ArticleDOI

Inositol trisphosphate and calcium signalling

TL;DR: Inositol trisphosphate is a second messenger that controls many cellular processes by generating internal calcium signals through receptors whose molecular and physiological properties closely resemble the calcium-mobilizing ryanodine receptors of muscle.
Journal ArticleDOI

Inositol trisphosphate, a novel second messenger in cellular signal transduction.

TL;DR: Diacylglycerol operates within the plane of the membrane to activate protein kinase C, whereas inositol trisphosphate is released into the cytoplasm to function as a second messenger for mobilizing intracellular calcium.
Journal ArticleDOI

A model for receptor-regulated calcium entry

TL;DR: A capacitative model is proposed for the mechanism by which activation of surface membrane receptors causes sustained Ca2+ entry into cells from the extracellular space, which allows forCa2+ release and Ca2-mobilization to be controlled by a single messenger, inositol (1,4,5) trisphosphate.
Journal ArticleDOI

Release of Ca2+ from a nonmitochondrial intracellular store in pancreatic acinar cells by inositol-1,4,5-trisphosphate.

TL;DR: It is reported here that micromolar concentrations of Ins1,4,5P3 release Ca2+ from a nonmitochondrial intracellular Ca2- store in pancreatic acinar cells, and the results strongly suggest that this is the same Ca1+ store that is released by acetylcholine.
Journal ArticleDOI

Calcium sparks: elementary events underlying excitation-contraction coupling in heart muscle

TL;DR: The calcium spark is the consequence of elementary events underlying excitation-contraction coupling and provides an explanation for both spontaneous and triggered changes in the intracellular calcium concentration in the mammalian heart.
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