Gene interactions and pathways from curated databases and text-mining

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AKT3 — PDPK1

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: AKT3 → PDPK1 (directlyIncreases, PDPK1 Activity, AKT3 Activity)
    Evidence: identified four sites (Ser-124, Thr-308, Thr-450, and Ser-473) on Akt1 that are phosphorylated in vivo. Thr-308 and Ser-473 are inducibly phosphorylated after treatment of cells with extracellular stimuli, whereas Ser-124 and Thr-450 appear to be basally phosphorylated The third mechanism by which 3'-phosphorylated phosphoinositides regulate Akt activity is by controlling the accessibility of Akt as a substrate for PDKs. In in vitro reconstitution assays, the binding of PI3,4,5P to the Akt PH do...
  • KEGG mTOR signaling pathway: PDPK1 → AKT1/AKT2/AKT3 (protein-protein, phosphorylation)
  • KEGG Focal adhesion: PDPK1 → AKT1/AKT2/AKT3 (protein-protein, phosphorylation)
  • KEGG Insulin signaling pathway: PDPK1 → AKT1/AKT2/AKT3 (protein-protein, activation)
  • KEGG Endometrial cancer: PDPK1 → AKT1/AKT2/AKT3 (protein-protein, activation)
  • KEGG Prostate cancer: PDPK1 → AKT1/AKT2/AKT3 (protein-protein, activation)
  • KEGG Non-small cell lung cancer: PDPK1 → AKT1/AKT2/AKT3 (protein-protein, activation)
  • KEGG Non-small cell lung cancer: PDPK1 → AKT1/AKT2/AKT3 (protein-protein, activation)
  • WikiPathways Focal Adhesion-PI3K-Akt-mTOR-signaling pathway: PDPK1 → AKT1/AKT3/AKT2 (activation)
  • WikiPathways Focal Adhesion: PDPK1 → AKT1/AKT2/AKT3 (activation)
  • WikiPathways Integrin-mediated Cell Adhesion: PDPK1 → AKT1/AKT2/AKT3 (activation)
  • WikiPathways Signaling Pathways in Glioblastoma: PDPK1 → AKT1/AKT2/AKT3 (mim-stimulation)

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *