{
 "meta": {
  "api_version": "1.0.0",
  "dataset_version": "2.0.1+unreleased",
  "live_matches_release": false,
  "archived_release": {
   "version": "2.0.1",
   "version_doi": "10.5281/zenodo.23090261",
   "date": "2026-10-01",
   "studies": 428
  },
  "data_fingerprint": "4823f516b720e66843f0b75952daf5ccc5279a7c20c0cb7c0d1ac126ff6ca768",
  "corpus_snapshot": "2026-10-24T21:34:23+0200",
  "source_commit": "8f0f14a10e115daab72bb59e5bf8c63eda1daeb8",
  "license": "CC-BY-4.0",
  "cite": "Barton O. Oliver's mTOR Atlas (live data, not an archived version; give corpus_snapshot and source_commit). doi:10.5281/zenodo.22059963",
  "docs": "https://mtor-atlas.org/api/"
 },
 "data": {
  "id": "MTORC2-AKT",
  "claim": "mTORC2 activates Akt/PKB",
  "source": {
   "name": "mTORC2",
   "entity": "mtorc2"
  },
  "target": {
   "name": "Akt/PKB",
   "entity": "akt-pkb"
  },
  "effect": "activates",
  "type": "phosphorylation",
  "directness": "direct",
  "timescale": "seconds",
  "compartment": "pm",
  "map_band": "pm",
  "species": [
   "mammalian cells"
  ],
  "mechanism": "mTORC2 puts the second, activating phosphate on Akt (Ser473). This is the step rapamycin eventually breaks, and a major reason, in mice, that chronic rapamycin impairs glucose tolerance (LAM2012).",
  "mechanism_beginner": "mTORC2 adds the final activating tag to Akt – the same step that long-term use of the drug rapamycin eventually disrupts. In mice, that disruption is a major reason long-term rapamycin raises blood sugar.",
  "context": "S473 contribution to Akt output is substrate-dependent: some Akt substrates are strongly mTORC2-dependent, others barely.",
  "boundary": "Mammalian cell studies, cancer cells and one mouse and rat liver study (ARI2015). Ser473 phosphorylation is shown in cells. The glucose consequence of losing it comes from mouse work (LAM2012) and has not been measured in people.",
  "boundary_tags": [],
  "note": "Bridge edge between the growth-factor route and the rapamycin route.",
  "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": [
    "JAC2006",
    "FRI2006",
    "YAN2006",
    "LIU2015",
    "ROD2011",
    "ARI2015",
    "GAN2011",
    "FAC2008",
    "HAG2012"
   ],
   "conflicting": []
  },
  "external_refs": [],
  "reviewed": null,
  "updated": null,
  "checked": null,
  "review_status": "unreviewed",
  "reviewer": null,
  "curation_status": "Proposed",
  "url": "https://mtor-atlas.org/relation/MTORC2-AKT/",
  "api_url": "https://mtor-atlas.org/api/v1/relations/MTORC2-AKT.json"
 }
}