Both increases in the basal cytosolic calcium concentration ([Ca2+]cyt) and [Ca2+]cyt transients play a major role
in cell cycle progression, cell proliferation and division. Calcium influx and release from endoplasmic reticulum are the
major routes involved in the variations in [Ca2+]cyt and past studies have clearly shown that calcium influx controls cell
growth and proliferation in several cell types. Furthermore, various studies in the past thirty years have demonstrated that
calcium channel expression levels, as well as cell specific expression, were determinant in these physiological processes.
Cell proliferation is directly linked to cell cycle progression, and again, it became evident that calcium channel expression
interferes here. It is also clear that calcium influx and cell proliferation relationship can be uncoupled in transformed and
cancer cells, resulting in an external calcium-independent proliferation. Other divalent cations such as iron and zinc involved
in cell proliferation permeating some calcium channels may interfere in this cellular process. This patent review is
focused on transient receptor potential and ORAI channels, and, as calcium influx regulates several other transduction
pathways, we assume that specific signalization complexes are needed to trigger activation of proliferation and cell division
in mammalian cells.
Keywords: Calcium channels, cell cycle, cell proliferation, cyclins, mitosis, ORAI, SERCA, TRPC
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