IndraLab

Statements

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"In addition, USP38 attenuated cellular ROS and suppressed cell apoptosis under hypoxia."
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"Knockout of USP38 hindered cancer cell proliferation, migration, and invasion, and enhanced apoptosis."
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"For instance, USP38 stabilizes HIF1α through deubiquitination under hypoxic conditions, thereby reducing cellular ROS and inhibiting apoptosis [20]."
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"By stabilizing MCT1, USP38 facilitates lactate export, thereby preventing intracellular lactate accumulation and reducing apoptosis.3.7 USP38 Activated the AKT/mTOR Pathway to Inhibit PM2.5-Induced Apoptosis."
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"Loss of USP38 leads to accumulation of cellular ROS and increased cell apoptosis."
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"Knockdown of USP38 enhanced PM2.5‐induced cell apoptosis (Figure 2D and Figure S1D) and led to increased lactate accumulation (Figure 2F)."
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"However, the underlying mechanisms are still poorly understood and need to be further explored.In this study, we found that knockout of USP38 resulted in the accumulation of ROS and increased cell apoptosis."
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