Q9V3Y8 is the selected 720-residue IKKepsilon/Ik2 sequence with its kinase domain at residues 12–317. Primary fly studies independently establish Spn-F, Nuf and DIAP1 phosphorylation: PMID:18796167(https://pubmed.ncbi.nlm.nih.gov/18796167/), PMID:21316589(https://pubmed.ncbi.nlm.nih.gov/21316589/) and PMID:16887178(https://pubmed.ncbi.nlm.nih.gov/16887178/). The broad ProtNLM reaction is CNN. Full texts inspected include the Spn-F kinase study, Rab interactome, bristle-localization study and SOP timing study.
PMID:34965418(https://pubmed.ncbi.nlm.nih.gov/34965418/) full text directly depletes dTBK1/Ik2 in enterocytes and establishes STING-dependent antiviral signaling. The type-I-interferon IBA is nevertheless invalid: PMID:30119996(https://pubmed.ncbi.nlm.nih.gov/30119996/) explicitly describes flies as devoid of interferons. This distinguishes conserved antiviral pathway activity from a taxon-incompatible downstream response.
The original apoptosis paper remains abstract-only and is not overruled from its nonapoptotic title; the apoptosis annotation is UNDECIDED. By contrast, PMID:19822670(https://pubmed.ncbi.nlm.nih.gov/19822670/) full text explicitly places the observed Ik2 effect after division and finds no phase-I change, so its SOP-cell-division annotation is overannotated. All 36 GOA rows are retained and reviewed.
The selected frozen UniProt record is retained in IKKepsilon-uniprot-source.json, with the complete original prediction metadata in IKKepsilon-predictions-source.json. It maps the exact accession to this FlyBase gene; current sequence identity does not establish the historical predictor input. Gene-level experiments support conserved functions unless a relevant isoform difference is established. Falcon research was requested with perplexity-lite fallback alongside publication caching. Primary publications and sequence observations, rather than AI summaries or ARBA assertions, support the curated conclusions.
The completed Falcon report was inspected. It correctly distinguishes Ik2 from Ird5, but its claim that DIAP1 direct phosphorylation is not established conflicts with the explicit primary PMID:16887178 abstract and later full-paper descriptions. The primary source is retained as the evidential basis. The report also misses the enterocyte-specific dTBK1/STING antiviral mechanism established by full PMID:34965418; the review includes that target-specific evidence.