Departure gate of acidic Ca2+ confirmed |
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| Authors: | Thomas J Jentsch Maja B Hoegg-Beiler Janis Vogt |
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| Affiliation: | 1Department Physiology and Pathology of Ion Transport, Leibniz-Institut für Molekulare Pharmakologie (FMP), Berlin, Germany;2Max-Delbrück-Centrum für Molekulare Medizin (MDC) in der Helmholtz Gemeinschaft, Berlin, Germany;3NeuroCure Cluster of Excellence, Charité Universitätsmedizin Berlin, Berlin, Germany |
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| Abstract: | More potent, but less known than IP3 that liberates Ca2+ from the ER, NAADP releases Ca2+ from acidic stores. The notion that TPC channels mediate this Ca2+ release was questioned recently by studies suggesting that TPCs are rather PI(3,5)P2‐activated Na+ channels. Ruas et al (2015) now partially reconcile these views by showing that TPCs significantly conduct both cations and confirm their activation by both NAADP and PI(3,5)P2. They attribute the failure of others to observe TPC‐dependent NAADP‐induced Ca2+ release in vivo to inadequate mouse models that retain partial TPC function. |
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