Browse our anti-PIK3C3 (PIK3C3) Antibodies

Zebrafish Phosphoinositide-3-Kinase, Class 3 (PIK3C3) interaction partners

1. These results not only reveal a role of PIK3C3 in gut homeostasis, but also provide a zebrafish inflammatory bowel disease model.

Human Phosphoinositide-3-Kinase, Class 3 (PIK3C3) interaction partners

1. Ribophagic flux was not induced upon inhibition of translational elongation or nascent chain uncoupling, but was induced in a comparatively selective manner under proteotoxic stress induced by arsenite (10) or chromosome mis-segregation (11) , dependent upon VPS34 and ATG8 conjugation

2. Vps34 stimulates tumor development mainly through PKC-delta- activation of p62.

3. Here we show that a putative fifth subunit, nuclear receptor binding factor 2 (NRBF2), is a tightly bound component of the class III phosphatidylinositol 3-kinase complex I that profoundly affects its activity and architecture. NRBF2 is a homodimer and drives the dimerization of the larger PI3KC3-C1 complex, with implications for the higher-order organization of the preautophagosomal structure.

4. 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.

5. Atg38 and its human ortholog NRBF2, accessory components of complex I consisting of Vps15-Vps34-Vps30/Atg6-Atg14 (yeast) and PIK3R4/VPS15-PIK3C3/VPS34-BECN1/Beclin 1-ATG14 (human), were characterized.

6. 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.

7. Low VPS34 expression is associated with cancer.

8. Arf tumor suppressor as a new transcriptional target of nuclear EGFR and highlight Vps34 as an important regulator of the nuclear EGFR/Arf survival pathway.

9. Vps34 has a previously unknown role in regulating Rab7 activity and late endosomal trafficking.

10. High expression of VPS34 promoted GRP78 transcription by modulating ATF6. VPS34 could enhance GRP78 protein stability.

11. These results establish Vps34 as an essential determinant of both short-term and long-term canonical GPCR signaling.

12. 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.

13. cis-unsaturated fatty acids require neither BECN1 nor PIK3C3 to stimulate the autophagic flux

14. tubulation requires mTOR activity, and we identified two direct mTOR phosphorylation sites on UVRAG (S550 and S571) that activate VPS34.

15. High expression of PI3K core complex genes is associated with poor prognosis in chronic lymphocytic leukemia.

16. reveal a novel function of GABP in the regulation of autophagy via transcriptional activation of the BECN1-PIK3C3 complex

17. Data indicte that Compound 31 constitutes an optimized class III phosphoinositide 3-kinase Vps34 inhibitor that could be used to investigate cancer biology.

18. VPS34-IN1 will provide a useful tool to decipher the kinase-dependent functions of Vps34, with acute changes in SGK3 phosphorylation and subcellular localization being new biomarkers of Vps34 activity.

19. DNA damage regulates Vps34 complexes and its downstream mechanisms, including autophagy and receptor endocytosis, through SCF (Skp1-Cul1-F-box)-mediated ubiquitination and degradation

20. Insulin can spatially regulate VPS34 activity through Src-mediated tyrosine phosphorylation.

Pig (Porcine) Phosphoinositide-3-Kinase, Class 3 (PIK3C3) interaction partners

1. These results suggest that LEPR, MC4R, PIK3C3 and VRTN are useful markers for accurately predicting breeding values in Duroc pigs.

2. confirmed that the polymorphism in PIK3C3 (C2604T) has the potential to be a genetic marker for production traits in Duroc pigs

Mouse (Murine) Phosphoinositide-3-Kinase, Class 3 (PIK3C3) interaction partners

1. results suggest that altered adipose tissue characteristics due to Pik3c3 knock out early in life has beneficial effects that promote adipose tissue browning and improves glucose tolerance in late-life.

2. In mouse liver, Vps34 inactivation mildly dampens autophagy, limiting substrate availability for mitochondrial respiration and reducing gluconeogenesis.

3. 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.

4. 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.

5. 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.

6. Phosphatidylinositol-3-phosphate is light-regulated, and Vps34 is essential for survival of retinal rod photoreceptor cells.

7. 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.

8. 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.

9. 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.

10. 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.

11. Vps34 has a previously unknown role in regulating Rab7 activity and late endosomal trafficking.

12. PIK3C3 was strongly expressed in the axon of cortical neurons during brain development.

13. provide the novel evidence that GADD45A inhibits autophagy via impairing the BECN1-PIK3C3 complex formation

14. PAQR3 controls autophagy by integrating AMPK signaling to enhance ATG14L-associated PI3K activity

15. Depletion of hepatic Vps15, the regulatory subunit of class III PI3K, increases insulin sensitivity and Akt signaling.

16. 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.

17. Beclin 1 regulates endosome pathways via the UVRAG-VPS34 complex.

18. Class III PI3K plays a central role in the transition of cardiac hypertrophy to heart failure via a prolonged activation of autophagy.

19. tubulation requires mTOR activity, and we identified two direct mTOR phosphorylation sites on UVRAG (S550 and S571) that activate VPS34.

20. These data reveal a key role for NRBF2 in the assembly of the specific Atg14L-Beclin 1-Vps34-Vps15 complex for autophagy induction.