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This is a presentation on modeling calcium signals,
understanding calcium regulatory networks in cells.
My name is David Friel from the Department of Neurosciences at Case Western Reserve University.
My research focuses on calcium signaling in excitable cells,
most recently focusing on the impact of calcium channel mutations on chemical
and electrical signaling, in cells within the cerebellar cortex that participate in motor control.
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Calcium is important in all cells, where it serves both as a charge carrier, and
as a chemical signal that regulates a variety of cellular processes.
As a chemical signal, calcium acts by binding to, and altering the state of, various effector proteins.
For this rôle, the level of binding site occupancy is critical.
Binding site occupancy depends on two things:
intrinsic properties of calcium-binding proteins,
which dictate how rapidly they bind and unbind calcium;
and the free calcium concentration and its history.
Given the importance of the free calcium concentration,
it's not surprising that it is tightly regulated.
For this purpose, cells use a variety of channels, pumps and exchangers -
referred to here collectively as 'transporters' -
to control it both spatially and temporally.
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There are two fundamental questions in calcium-signaling research.
First, how are calcium signals produced?
More specifically, what determines the evolution of the calcium concentration in time and space?
Second, once they are produced, how are calcium signals translated into cellular effects?
In this presentation, we will be concerned mainly with question number one.
The listener is referred to other presentations in this series for
a discussion of physiological processes that are regulated by calcium,
such as muscle contraction, secretion, membrane excitability, gene expression, and so on.
