{
 "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": "LKB1-AMPK",
  "claim": "LKB1 (STK11) activates AMPK",
  "source": {
   "name": "LKB1 (STK11)",
   "entity": "lkb1-stk11"
  },
  "target": {
   "name": "AMPK",
   "entity": "ampk"
  },
  "effect": "activates",
  "type": "phosphorylation",
  "directness": "direct",
  "timescale": "seconds",
  "compartment": "cytosol",
  "map_band": "cytosol",
  "species": [
   "mammalian cells"
  ],
  "mechanism": "LKB1 is the main kinase that primes AMPK, phosphorylating AMPK-alpha directly on Thr172; in LKB1-null cells AMPK no longer responds to energy stress (SHW2004). It is not the only upstream kinase: CaMKK2 phosphorylates the same site when calcium rises, and LKB1-deficient cells keep some basal AMPK activity (Hawley 2005, PMID 16054095; Woods 2005, PMID 16054096; outside this corpus).",
  "mechanism_beginner": "LKB1 is the main switch that turns AMPK on when energy runs low; in cells without it, AMPK no longer responds to low energy. A second kinase can still switch AMPK on when calcium rises, so AMPK is not completely silent.",
  "context": null,
  "boundary": "Canonical step, established in LKB1-null cells and in vitro kinase assays (SHW2004). Coded M – molecular – because that is what the supporting evidence is: cell and in vitro biochemistry, not an organismal phenotype.",
  "note": "2026-10-10: 'without it the whole energy-stress arm is deaf' / 'the whole alarm system goes silent' narrowed. LKB1 loss removes the response to energy stress, not all AMPK activity (CaMKK2 arm, Hawley 2005 / Woods 2005).",
  "consensus_contested": false,
  "curation_contested": false,
  "contested": false,
  "confidence": {
   "mechanistic": "high",
   "human_relevance": "plausible",
   "consensus": "established"
  },
  "evidence": {
   "kind": "Genetic epistasis",
   "strongest": {
    "code": "M",
    "label": "Molecular — cells, biochemistry, structure"
   },
   "supporting": [
    "SHW2004"
   ],
   "conflicting": []
  },
  "external_refs": [
   {
    "pmid": "16054095",
    "cited_in": [
     "mechanism"
    ],
    "in_corpus": false,
    "url": "https://pubmed.ncbi.nlm.nih.gov/16054095/"
   },
   {
    "pmid": "16054096",
    "cited_in": [
     "mechanism"
    ],
    "in_corpus": false,
    "url": "https://pubmed.ncbi.nlm.nih.gov/16054096/"
   }
  ],
  "reviewed": null,
  "updated": null,
  "checked": null,
  "review_status": "unreviewed",
  "reviewer": null,
  "curation_status": "Proposed",
  "url": "https://mtor-atlas.org/relation/LKB1-AMPK/",
  "api_url": "https://mtor-atlas.org/api/v1/relations/LKB1-AMPK.json"
 }
}