{
 "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": "MTORC1-SENESCENCE",
  "claim": "mTORC1 activates Senescence-associated secretory phenotype (SASP)",
  "source": {
   "name": "mTORC1",
   "entity": "mtorc1"
  },
  "target": {
   "name": "Senescence-associated secretory phenotype (SASP)",
   "entity": "senescence-associated-secretory-phenotype-sasp"
  },
  "effect": "activates",
  "type": "functional-consequence",
  "directness": "indirect",
  "timescale": "days",
  "compartment": null,
  "map_band": "outcome",
  "species": [
   "mammalian cells"
  ],
  "mechanism": "mTORC1 sustains the inflammatory secretory output of cells that are already senescent, by promoting IL1A translation. Inhibiting it quietens that output without reversing the proliferative arrest.",
  "mechanism_beginner": "mTORC1 keeps old, \"senescent\" cells pumping out inflammatory signals, and blocking it calms that output down without making those cells young again. Whether mTORC1 also helps push cells into senescence in the first place is a separate question this arrow does not answer.",
  "context": null,
  "boundary": "Three studies, all in cells or a rat disease model. LAB2015 and NAR2011 measure the secretory output of cells that are already senescent (IL1A translation; IL-6/IL-8 production fuelled by mTOR at the TASCC). CHEN2026C (human disc cells, rat needle-puncture model) shows mTORC1 hyperactivation after TSC2 loss together with senescence and SASP, both blocked by rapamycin - a disease-model result, not a general demonstration that mTORC1 drives cells into senescence. That is why this arrow lands on the secretory programme and not on senescence itself.",
  "note": "The arrow means mTORC1 sustains the secretory output (SASP) of senescent cells. Whether mTORC1 also pushes cells into senescence in the first place (geroconversion) is a separate and weaker claim that this edge does not make.",
  "consensus_contested": false,
  "curation_contested": false,
  "contested": false,
  "confidence": {
   "mechanistic": "medium",
   "human_relevance": "plausible",
   "consensus": "emerging"
  },
  "evidence": {
   "kind": "Genetic epistasis",
   "strongest": {
    "code": "A",
    "label": "Animal model"
   },
   "supporting": [
    "LAB2015",
    "CHEN2026C",
    "NAR2011"
   ],
   "conflicting": []
  },
  "external_refs": [],
  "reviewed": null,
  "updated": null,
  "checked": null,
  "review_status": "unreviewed",
  "reviewer": null,
  "curation_status": "Proposed",
  "url": "https://mtor-atlas.org/relation/MTORC1-SENESCENCE/",
  "api_url": "https://mtor-atlas.org/api/v1/relations/MTORC1-SENESCENCE.json"
 }
}