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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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Across all of the dose levels, 28% of the trial participants discontinued treatment, compared to 18% of placebo subjects

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