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FUNDING This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korean government (MSIT) RS-2023-00208709 (to Kyu Chang Won) and a grant from the Korea government’s Institute of Information and Communications Technology Planning & Evaluation (IITP) (RS-2022-II220965), Development of diabetes patient’s healthcare digital twin technology based on continuous lifelog variables
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922 In AKT-hyperactivated cancer cells, AKT directly phosphorylates the Ser343 site of TRPML1, inhibits the K552 ubiquitination degradation of TRPML1, and promotes the binding of TRPML1 to ARL8B, leading to lysosomal exocytosis
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