The inositol 1,4,5-trisphosphate receptor (IP₃R) is one of two Ca²⁺ channels that gates Ca²⁺ release from ER-stores. The ligand IP₃, generated upon specific G-protein coupled receptor activation, binds to IP₃R to release Ca²⁺ into the cytosol. IP₃R also mediates ER-store Ca²⁺ release into the mitochondria, under basal as well as stimulatory conditions; an activity that influences cellular bioenergetics and thus, cellular growth and proliferation. In Drosophila neuroendocrine cells expressing a hypomorphic mutant of IP₃R, we observed reduced protein translation levels. Here, we discuss the possible molecular mechanism for this observation. We hypothesize that the cellular energy sensor, AMPK connects IP₃R mediated Ca²⁺ release into the mitochondria, to protein translation, via the TOR pathway.

肌醇 1,4,5-三磷酸受体 (IP ₃ R) 是控制 ER 库释放 Ca ²⁺的两个 Ca ²⁺通道之一。特定G蛋白偶联受体激活后产生的配体IP ₃与IP ₃ R 结合，将Ca ²⁺释放到细胞质中。在基础和刺激条件下，IP ₃ R 还介导 ER 储存 Ca ²⁺释放到线粒体中；一种影响细胞生物能量学从而影响细胞生长和增殖的活动。在表达 IP ₃ R 亚形突变体的果蝇神经内分泌细胞中，我们观察到蛋白质翻译水平降低。在这里，我们讨论了这一观察结果可能的分子机制。我们假设细胞能量传感器 AMPK 通过 TOR 途径将 IP ₃ R 介导的 Ca ²⁺释放到线粒体中与蛋白质翻译连接起来。