IndraLab

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ZRANB1 activates PIK3C3. 8 / 8
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"Thus, our results highlight the importance of TRABID mediated VPS34 stabilization in maintaining normal liver metabolism and uncover the contribution of TRABID downregulation to the pathogenesis of liver steatosis through VPS34 destabilization and autophagy deficiency."
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"TRABID knockdown decreased VPS34 protein abundance and half-life, whereas TRABID overexpression enhanced VPS34 expression and stability."
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"To interrogate the in vivo function of TRABID mediated VPS34 stabilization in liver metabolism, we set up a mouse model of nonalcoholic fatty liver disease (NAFLD) via feeding mice with a high-fat diet (HFD)."
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"We provide evidence that this switch of UBE3C localization plays a critical role for cells to cope with the stressed conditions by favoring TRABID mediated VPS34 stabilization and autophagy induction, as prevention of this switch by an enforced association of UBE3C with VPS34 impairs autophagy and compromises proteostasis, ER quality control and cell survival."
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"Specifically in the liver, we show that TRABID mediated VPS34 stabilization is critical for lipid metabolism and is downregulated during the pathogenesis of steatosis."
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"In the liver, TRABID mediated VPS34 stabilization is important for lipid metabolism and is downregulated in a mouse model of NAFLD."
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"Our findings suggest that the balance between UBE3C and TRABID on VPS34 regulation is disturbed by various ER/proteotoxic stressors to favor TRABID mediated VPS34 stabilization, thus facilitating autophagy induction."
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"We next investigated the functional consequence of TRABID mediated VPS34 deubiquitnation."
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