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In mouse liver, Vps34 inactivation mildly dampens autophagy, limiting substrate availability for mitochondrial respiration and reducing gluconeogenesis.
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AP-1/sigma1A-ArfGAP1-Rabex-5 complex formation leads to more endosomal Rabex-5 and enhanced, Rab5(GTP)-stimulated Vps34 PI3-kinase activity, which is essential for multivesicular body endosome formation.
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dendritic cells from Vps34-deficient mice have a partially activated phenotype, spontaneously produce cytokines, and exhibit enhanced activity of the classic MHC class I and class II antigen-presentation pathways and displayed a defect in the homeostatic maintenance of splenic CD8alpha(+) dendritic cells and in the capacity of these cells to cross-present cell corpse-associated antigens to MHC class I-restricted T cells.
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Results demonstrate that Vps34 is essential for proper myelination by Schwann cells. Depletion of PI3P leads to enlarged late endosomal/lysosomal vacuoles and suppressed trafficking in Schwann cells. Suppressed endosomal trafficking likely causes changes in the abundance and post-translational modification of ErbB2/3, a signaling defect that may contribute to arrested myelination in Vps34 deficient nerves.
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Phosphatidylinositol-3-phosphate is light-regulated, and Vps34 is essential for survival of retinal rod photoreceptor cells.
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This study reveals NRBF2 as a critical molecular switch of PtdIns3K and autophagy activation, and its on/off state is precisely controlled by MTORC1 through phosphorylation.
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This study uncovers a dual role for Vps34 as a regulator of platelet production by megakaryocytes and as an unexpected regulator of platelet activation and arterial thrombus formation dynamics.
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E. chaffeensis secretes Etf-1 to induce autophagy to repurpose the host cytoplasm and capture nutrients for its growth through RAB5 and class III PtdIns3K, while avoiding autolysosomal killing.
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p300-dependent VPS34 acetylation/deacetylation is the physiological key to VPS34 activation, which controls the initiation of canonical autophagy and of non-canonical autophagy in which the upstream kinases of VPS34 can be bypassed.
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Vps34 has a previously unknown role in regulating Rab7 activity and late endosomal trafficking.
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PIK3C3 was strongly expressed in the axon of cortical neurons during brain development.
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provide the novel evidence that GADD45A inhibits autophagy via impairing the BECN1-PIK3C3 complex formation
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PAQR3 controls autophagy by integrating AMPK signaling to enhance ATG14L-associated PI3K activity
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Depletion of hepatic Vps15, the regulatory subunit of class III PI3K, increases insulin sensitivity and Akt signaling.
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Study identifies a key role of Cul3-KLHL20 in autophagy termination by controlling autophagy-dependent turnover of ULK1 and VPS34 complex subunits and reveals the pathophysiological functions of this autophagy termination mechanism.
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Beclin 1 regulates endosome pathways via the UVRAG-VPS34 complex.
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Class III PI3K plays a central role in the transition of cardiac hypertrophy to heart failure via a prolonged activation of autophagy.
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tubulation requires mTOR activity, and we identified two direct mTOR phosphorylation sites on UVRAG (S550 and S571) that activate VPS34.
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These data reveal a key role for NRBF2 in the assembly of the specific Atg14L-Beclin 1-Vps34-Vps15 complex for autophagy induction.
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Vps34 is a main phosphatidylinositol 3-phosphate source for constitutive PIKfyve functionality.
