Immunocyte Ca <sup>2+</sup> Influx System Mediated by LTRPC2
Yorikata Sano(Drug Discovery Laboratory (Norway)), Kohei Inamura(Drug Discovery Laboratory (Norway)), Akira Miyake(Drug Discovery Laboratory (Norway)), Shinobu Mochizuki(Drug Discovery Laboratory (Norway)), Hiromichi Yokoi(Drug Discovery Laboratory (Norway)), Hitoshi Matsushime(Drug Discovery Laboratory (Norway)), Kiyoshi Furuichi(Drug Discovery Laboratory (Norway))
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Abstract
We characterized an activation mechanism of the human LTRPC2 protein, a member of the transient receptor potential family of ion channels, and demonstrated that LTRPC2 mediates Ca2+ influx into immunocytes. Intracellular pyrimidine nucleotides, adenosine 5'-diphosphoribose (ADPR), and nicotinamide adenine dinucleotide (NAD), directly activated LTRPC2, which functioned as a Ca2+-permeable nonselective cation channel and enabled Ca2+ influx into cells. This activation was suppressed by intracellular adenosine triphosphate. These results reveal that ADPR and NAD act as intracellular messengers and may have an important role in Ca2+ influx by activating LTRPC2 in immunocytes.
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