Gene name: phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit gamma
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PMID |
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1 |
26893923
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Angiotensin II induces endoplasmic reticulum stress in podocyte, which would be further augmented by PI3-kinase inhibition.
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2 |
26825532
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Deletion of a key endosomal trafficking regulator, the class 3 phosphatidylinositol (PtdIns) 3-kinase vacuolar protein sorting 34 (Vps34), in podocytes results in aberrant endosomal membrane morphology and podocyte dysfunction.
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3 |
26825532
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We recently showed that the vacuolation phenotype in cultured Vps34-deficient podocytes is caused by the absence of a substrate for the Vps34 downstream effector PtdIns 3-phosphate 5-kinase (PIKfyve), which phosphorylates Vps34-generated PtdIns(3)P to produce PtdIns (3,5)P2.
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4 |
25448064
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We report that in mouse islet β-cells and the mouse pancreatic beta-cell line (βTC-6 cells) nephrin is associated and partly co-localized with PI3-kinase.
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5 |
25448064
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We report that in mouse islet β-cells and the mouse pancreatic beta-cell line (βTC-6 cells) nephrin is associated and partly co-localized with PI3-kinase.
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6 |
25448064
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Incubation of cells with functional anti-nephrin antibodies induced nephrin clustering at the plasma membrane, nephrin phosphorylation and recruitment of PI3-kinase to nephrin thus resulting in increased PI3K-dependent Akt phosphorylation and augmented phosphorylation/inhibition of pro-apoptotic Bad and FoxO.
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7 |
25448064
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Incubation of cells with functional anti-nephrin antibodies induced nephrin clustering at the plasma membrane, nephrin phosphorylation and recruitment of PI3-kinase to nephrin thus resulting in increased PI3K-dependent Akt phosphorylation and augmented phosphorylation/inhibition of pro-apoptotic Bad and FoxO.
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8 |
25448064
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Nephrin silencing abolished Akt activation and increased susceptibility of cells to apoptosis.
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9 |
25448064
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Nephrin silencing abolished Akt activation and increased susceptibility of cells to apoptosis.
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10 |
25448064
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Interestingly, a marked decrease in nephrin expression and phosphorylated Akt was observed in pancreatic islets of db/db lepr-/- diabetic mice.
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11 |
25448064
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Interestingly, a marked decrease in nephrin expression and phosphorylated Akt was observed in pancreatic islets of db/db lepr-/- diabetic mice.
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12 |
23614954
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The class III phosphatidylinositol 3-kinase PIK3C3/VPS34 regulates endocytosis and autophagosome-autolysosome formation in podocytes.
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13 |
23614954
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In mammalian cells, the evolutionarily conserved class III PtdIns 3-kinase PIK3C3/VPS34 is part of a large multiprotein complex that catalyzes the localized phosphorylation of phosphatidylinositol to phosphatidylinositol-3-phosphate (PtdIns3P).
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14 |
23518611
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PIK3C3/VPS34, the class III PtdIns 3-kinase, plays indispensable roles in the podocyte.
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15 |
22534961
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Divergent roles of Smad3 and PI3-kinase in murine adriamycin nephropathy indicate distinct mechanisms of proteinuria and fibrogenesis.
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16 |
22534961
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Divergent roles of Smad3 and PI3-kinase in murine adriamycin nephropathy indicate distinct mechanisms of proteinuria and fibrogenesis.
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17 |
22534961
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Divergent roles of Smad3 and PI3-kinase in murine adriamycin nephropathy indicate distinct mechanisms of proteinuria and fibrogenesis.
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18 |
22534961
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Divergent roles of Smad3 and PI3-kinase in murine adriamycin nephropathy indicate distinct mechanisms of proteinuria and fibrogenesis.
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19 |
22534961
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Renal Akt was phosphorylated in adriamycin-treated mice, suggesting PI3-kinase activation.
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20 |
22534961
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Renal Akt was phosphorylated in adriamycin-treated mice, suggesting PI3-kinase activation.
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21 |
22534961
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Renal Akt was phosphorylated in adriamycin-treated mice, suggesting PI3-kinase activation.
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22 |
22534961
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Renal Akt was phosphorylated in adriamycin-treated mice, suggesting PI3-kinase activation.
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23 |
22534961
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Expression of mRNA for the p110γ isozyme of PI3-kinase was specifically increased and p110γ colocalized with nephrin by immunohistochemistry early in disease.
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24 |
22534961
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Expression of mRNA for the p110γ isozyme of PI3-kinase was specifically increased and p110γ colocalized with nephrin by immunohistochemistry early in disease.
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25 |
22534961
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Expression of mRNA for the p110γ isozyme of PI3-kinase was specifically increased and p110γ colocalized with nephrin by immunohistochemistry early in disease.
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26 |
22534961
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Expression of mRNA for the p110γ isozyme of PI3-kinase was specifically increased and p110γ colocalized with nephrin by immunohistochemistry early in disease.
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27 |
22534961
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Thus, PI3-kinase p110γ mediates initial podocyte injury and proteinuria, both of which precede TGF-β-mediated glomerular scarring.
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28 |
22534961
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Thus, PI3-kinase p110γ mediates initial podocyte injury and proteinuria, both of which precede TGF-β-mediated glomerular scarring.
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29 |
22534961
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Thus, PI3-kinase p110γ mediates initial podocyte injury and proteinuria, both of which precede TGF-β-mediated glomerular scarring.
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30 |
22534961
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Thus, PI3-kinase p110γ mediates initial podocyte injury and proteinuria, both of which precede TGF-β-mediated glomerular scarring.
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31 |
15780083
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Insulin-like growth factors inhibit podocyte apoptosis through the PI3 kinase pathway.
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