ABSTRACT
Acknowledgments ................................................................................................ 411
References............................................................................................................. 411
Calcium is widely recognized as one of the most universal of intracellular signals,
and it controls a diverse array of cellular activities [1-3]. The commonest form of
intracellular Ca2þ signaling is triggered by extracellular agonists that bind to cell surface receptors that act through a variety of signal transduction pathways to
mobilize calcium either at the level of plasma membrane or intracellular calcium
channels. Numerous extracellular stimuli, acting through many classes of receptor
and ion channels, lead to increases in the cytosolic free Ca2þ concentration. Typically, cytosolic Ca2þ rises severalfold from resting values of ~100 nM to values as high as tens of micromolar. Once elevated, Ca2þ exerts its effects by influencing the activity of Ca2þ-dependent target proteins either directly or through
Ca2þ-binding proteins such as calmodulin [4, 5]. Multiple extrusion mechanisms exist within the cell to rapidly decrease Ca2þ, preventing the potentially toxic consequences of sustained Ca2þ elevations [6-8]. Ca2þ signals, thus, arise through the concerted activity of a variety of Ca2þ channels, pumps, and exchangers.
