An increasing number of studies based on recombinant cells and on mouse mod
els that express an altered repertoire of some of the key components of the
intracellular Ca2+ release stores are becoming available as a result of mo
lecular genetics techniques. Information from these studies, together with
results from studies of human diseases caused by mutations in genes that en
code proteins of the intracellular Ca2+ stores, are providing a significant
advancement in understanding the interactive nature of the molecular machi
nery that underlies intracellular Ca2+ signalling and how the different com
ponents of the Ca2+ stores contribute to the regulation of cellular functio
ns.