Triple

T19992590
Position Surface form Disambiguated ID Type / Status
Subject APOE gene E494100 entity
Predicate encodes P14248 FINISHED
Object apolipoprotein E NE NERFINISHED

How this triple was built (3 steps)

Every LLM step that produced this triple, in pipeline order — named-entity classification, the disambiguation choices (the exact options shown, with the pick highlighted), and the generated description. The batch + timestamp of each is in the Provenance table below.

NER Named-entity recognition gpt-5-mini
Instruction
Given a phrase, classify it is english named entity (e.g., persons, organizations, works of art) in Latin script, or not (e.g., literals, dates, URLs, verbose phrases). For disambiguation, the statement where the phrase occurs as object is also given. Please return a JSON object with `phrase` (string, the phrase being analyzed) and `is_ne` (boolean, indicating whether the phrase is a Named Entity).
Input
Phrase: apolipoprotein E | Statement: [APOE gene, encodes, apolipoprotein E]
NED1 Entity disambiguation (via context triple) gpt-5-mini-2025-08-07
Target entity: apolipoprotein E
Context triple: [APOE gene, encodes, apolipoprotein E]
  • A. APOE gene
    The APOE gene encodes apolipoprotein E, a key protein in lipid metabolism whose variants, especially ε4, strongly influence risk for Alzheimer’s disease and cardiovascular disorders.
  • B. APOE ε4 allele
    The APOE ε4 allele is a genetic variant of the apolipoprotein E gene that significantly increases an individual's susceptibility to late-onset Alzheimer's disease.
  • C. APOE ε3 allele
    The APOE ε3 allele is the most common and generally considered the “neutral” variant of the apolipoprotein E gene, associated with average risk for Alzheimer’s disease and typical lipid metabolism compared to other APOE alleles.
  • D. NPC1L1 transporter
    The NPC1L1 transporter is an intestinal membrane protein that mediates cholesterol absorption from the gut and is inhibited by the lipid-lowering drug ezetimibe.
  • E. Friedewald
    Friedewald is a small German locality historically associated with the nobility of Thuringia and Hesse.
  • F. None of above. chosen
  • G. Unsure - the case is ambiguous/there is not enough information to decide.
NED2 Entity disambiguation (via description) gpt-5-mini-2025-08-07
Target entity: apolipoprotein E
Target entity description: Apolipoprotein E is a lipid-transport protein in the blood whose genetic variants strongly influence cholesterol metabolism and risk for neurodegenerative and cardiovascular diseases, including Alzheimer’s disease.
  • A. APOE gene chosen
    The APOE gene encodes apolipoprotein E, a key protein in lipid metabolism whose variants, especially ε4, strongly influence risk for Alzheimer’s disease and cardiovascular disorders.
  • B. APOE ε4 allele
    The APOE ε4 allele is a genetic variant of the apolipoprotein E gene that significantly increases an individual's susceptibility to late-onset Alzheimer's disease.
  • C. APOE ε3 allele
    The APOE ε3 allele is the most common and generally considered the “neutral” variant of the apolipoprotein E gene, associated with average risk for Alzheimer’s disease and typical lipid metabolism compared to other APOE alleles.
  • D. NPC1L1 transporter
    The NPC1L1 transporter is an intestinal membrane protein that mediates cholesterol absorption from the gut and is inhibited by the lipid-lowering drug ezetimibe.
  • E. Friedewald
    Friedewald is a small German locality historically associated with the nobility of Thuringia and Hesse.
  • F. None of above.

Provenance (2 batches)

The batch behind each pipeline step, in order, with when it ran. Timestamps are batch-level — stages were processed in waves, so the object chain (NER → NED1 → NEDg → NED2) reads in order, but predicate / elicitation batches can sit in a different wave.

Step Stage Batch ID Status When
creating Elicitation batch_69da626a67648190af9653832a3aeced completed April 11, 2026, 3:02 p.m.
NER Named-entity recognition batch_69e65fe10ffc81908c94168b0a8ea9c9 completed April 20, 2026, 5:18 p.m.
Created at: April 11, 2026, 3:31 p.m.