Triple
T22516252
| Position | Surface form | Disambiguated ID | Type / Status |
|---|---|---|---|
| Subject | Cdc28 |
E556655
|
entity |
| Predicate | formsComplexWith |
P6653
|
FINISHED |
| Object | Cln3 |
—
|
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: Cln3 | Statement: [Cdc28, formsComplexWith, Cln3]
NED1
Entity disambiguation (via context triple)
gpt-5-mini-2025-08-07
Target entity: Cln3 Context triple: [Cdc28, formsComplexWith, Cln3]
-
A.
SOD1
SOD1 is a gene encoding the antioxidant enzyme superoxide dismutase 1, whose mutations are a major known cause of familial amyotrophic lateral sclerosis (ALS).
-
B.
C9orf72
C9orf72 is a human gene whose hexanucleotide repeat expansions are the most common known genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
-
C.
GRIN3A
GRIN3A is a gene that encodes a subunit of the N-methyl-D-aspartate (NMDA) receptor, a key glutamate-gated ion channel involved in synaptic transmission and plasticity in the central nervous system.
-
D.
GRIN3B
GRIN3B is a human gene that encodes the GluN3B subunit of NMDA-type glutamate receptors involved in excitatory neurotransmission and synaptic plasticity in the central nervous system.
-
E.
SMN complex
The SMN complex is a multiprotein assembly crucial for the biogenesis of small nuclear ribonucleoproteins (snRNPs) and proper pre-mRNA splicing, with key roles in motor neuron survival.
- 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: Cln3 Target entity description: Cln3 is a G1 cyclin in budding yeast that helps trigger the Start transition of the cell cycle by activating the Cdc28 cyclin-dependent kinase.
-
A.
SOD1
SOD1 is a gene encoding the antioxidant enzyme superoxide dismutase 1, whose mutations are a major known cause of familial amyotrophic lateral sclerosis (ALS).
-
B.
C9orf72
C9orf72 is a human gene whose hexanucleotide repeat expansions are the most common known genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
-
C.
GRIN3A
GRIN3A is a gene that encodes a subunit of the N-methyl-D-aspartate (NMDA) receptor, a key glutamate-gated ion channel involved in synaptic transmission and plasticity in the central nervous system.
-
D.
GRIN3B
GRIN3B is a human gene that encodes the GluN3B subunit of NMDA-type glutamate receptors involved in excitatory neurotransmission and synaptic plasticity in the central nervous system.
-
E.
SMN complex
The SMN complex is a multiprotein assembly crucial for the biogenesis of small nuclear ribonucleoproteins (snRNPs) and proper pre-mRNA splicing, with key roles in motor neuron survival.
- F. None of above. chosen
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_69e11e5657e881909f16ca58352c50da |
completed | April 16, 2026, 5:37 p.m. |
| NER | Named-entity recognition | batch_69f15e2cfc908190b3489228a1997f45 |
completed | April 29, 2026, 1:26 a.m. |
Created at: April 16, 2026, 8:50 p.m.