Selected horse accession: A0A3Q2HDT6. Source: ProtNLM2 API snapshot 2026-09-08, frozen in horse40-predictions.csv.
Binds to the IL-1 type I receptor following IL-1 engagement, triggering intracellular signaling cascades leading to transcriptional up-regulation and mRNA stabilization
Plausible, UNC for exact selected sequence. IRAK-M/IRAK3 can reconstitute IL-1 responses in an IRAK-deficient cell model, but is a signaling regulator rather than a conventional active receptor-associated kinase. The selected horse sequence lacks human residues 2–43, reaching the start of the death domain; intact receptor-complex assembly is therefore not established. The text also overstates direct receptor binding unless the receptor-associated complex is distinguished from a direct binary interaction. PMID:10383454(https://pubmed.ncbi.nlm.nih.gov/10383454/); DOI:10.1074/jbc.274.27.19403.
UNC. The positive IL-1-response result and negative physiological feedback are both real contexts. IRAK-M prevents IRAK/IRAK4 dissociation from MyD88 and restrains cytokine induction in knockout experiments. The prediction does not specify an assay context or identify which mRNAs are stabilized; a generic IRAK activator description is inadequate to establish these exact effects for horse IRAK3. PMID:12150927(https://pubmed.ncbi.nlm.nih.gov/12150927/); DOI:10.1016/s0092-8674(02)00827-9.
Human–horse sequence comparison records coverage, gaps and architecture caveats. Human experimental results support transfer where the relevant features are conserved; ARBA assertions and generated gene-review prose are not used as biological evidence. The human reference sequence and current horse sequence are not known to be the exact prediction-time inputs. Claim assessments are kept separate because a partly correct paragraph should not receive an undifferentiated verdict.