Search

Calcium plays a central role in cell signaling and T-type calcium channels constitute a unique route for the entry of calcium ions in excitable cells. The genuine electrophysiological properties of T-type calcium channels include activation at low voltages and window currents in the range of cell membrane resting potential. T-type channels therefore generate a specific calcium influx likely to play an important role during early stages of development, in various cellular functions including cell proliferation, cell differentiation, gene transcription and hormone secretion. Such T-channel activities are also associated with several pathological situations. With the recent cloning of three T-type pore channel subunits, alpha 1G, alpha 1H and alpha 1I (also called Cav3.1, Cav3.2 and Cav3.3, respectively), it has become possible to investigate further the role of T-type channels in various cellular functions, including neuronal differentiation. Here we describe recent data obtained in our laboratory demonstrating how T-type channels generated by the alpha 1H subunit contribute to neuronal differentiation.

Voltage-gated calcium channels are involved in a large variety of cellular functions such as excitation-contraction coupling, hormone secretion, firing and pacemaker activity, gene activation and proliferation. Cloning of complementary DNAs encoding for calcium channel subunits has challenged the study of the functional properties of calcium channels and has allowed analysis of the molecular basis of calcium channel diversity. Recently, pore-forming subunits of T-type calcium channels have been cloned. Recent data describing the genes encoding calcium channels, their molecular and pharmacological studies, as well as their linkage to human genetic diseases are reviewed in this article.

Three double mutants were prepared from single mutant chl-r strains of Escherichia coli K12 lacking nitrate reductase activity. When extracts of these three double mutants were mixed, nitrate reductase activity was reconstituted.