{
 "meta": {
  "api_version": "1.0.0",
  "dataset_version": "2.0.1",
  "corpus_snapshot": "2026-10-12T22:59:14+0200",
  "source_commit": "93739c9d195dc39e47eecfabc3cab2565a2f256f",
  "license": "CC-BY-4.0",
  "cite": "Barton O. Oliver's mTOR Atlas. doi:10.5281/zenodo.22059963",
  "docs": "https://mtor-atlas.org/api/"
 },
 "data": {
  "id": "AKT-TSC",
  "claim": "Akt/PKB inhibits TSC1/TSC2",
  "source": {
   "name": "Akt/PKB",
   "entity": "akt-pkb"
  },
  "target": {
   "name": "TSC1/TSC2",
   "entity": "tsc1-tsc2"
  },
  "effect": "inhibits",
  "type": "phosphorylation",
  "directness": "direct",
  "timescale": "seconds",
  "compartment": "cytosol",
  "map_band": "cytosol",
  "species": [
   "mammalian cells"
  ],
  "mechanism": "Akt phosphorylates TSC2, disabling the complex. Growth-factor signalling works by removing a brake, not by pressing an accelerator.",
  "mechanism_beginner": "Akt tags TSC2 to disable it. Growth signals work by releasing a brake, not by pressing a gas pedal.",
  "context": null,
  "boundary": "In mouse liver, Akt phosphorylation of TSC2 is the main route by which insulin switches on mTORC1, but feeding activates hepatic mTORC1 without it; that response needs dietary protein instead (KAL2026). The biochemical mechanism itself was shown in cultured human cells (INO2002).",
  "note": null,
  "consensus_contested": false,
  "curation_contested": false,
  "contested": false,
  "confidence": {
   "mechanistic": "high",
   "human_relevance": "plausible",
   "consensus": "established"
  },
  "evidence": {
   "kind": "Direct biochemical",
   "strongest": {
    "code": "A",
    "label": "Animal model"
   },
   "supporting": [
    "INO2002",
    "KAL2026",
    "LAP2026"
   ],
   "conflicting": []
  },
  "external_refs": [],
  "reviewed": null,
  "updated": null,
  "checked": null,
  "review_status": "unreviewed",
  "reviewer": null,
  "curation_status": "Proposed",
  "url": "https://mtor-atlas.org/relation/AKT-TSC/",
  "api_url": "https://mtor-atlas.org/api/v1/relations/AKT-TSC.json"
 }
}