Selected horse accession: A0A9L0T1D1. Source: ProtNLM2 API snapshot 2026-09-08, frozen in horse40-predictions.csv.
Receptor for a number of inflammatory CC-chemokines including CCL3/MIP-1-alpha, CCL4/MIP-1-beta and RANTES and subsequently transduces a signal by increasing the intracellular calcium ion level. May play a role in the control of granulocytic lineage proliferation or differentiation. Participates in T-lymphocyte migration to the infection site by acting as a chemotactic receptor
PLI. The human CXCR3-B study explicitly reports that these CC chemokines did not compete for radiolabeled CXCL10 binding. Its positive ligands were CXCL9/10/11 and CXCL4. The selected horse receptor is 90.8% identical across the full human CXCR3-A sequence with seven membrane helices retained. The stated ligand set is characteristic of a different chemokine-receptor specificity, not validated by the broad family label. PMID:12782716(https://pubmed.ncbi.nlm.nih.gov/12782716/); DOI:10.1084/jem.20021897.
COR. Human CXCR3 "mediates Ca2+ mobilization and chemotaxis in response to IP10 and Mig" (PMID:9064356(https://pubmed.ncbi.nlm.nih.gov/9064356/)), and CXCR3-A transfectants mediate calcium flux in response to CXCL9, CXCL10 and CXCL11 (PMID:12782716(https://pubmed.ncbi.nlm.nih.gov/12782716/); DOI:10.1084/jem.20021897). These results do not validate the incorrect ligand list in the preceding sentence. The selected horse product is 90.8% identical to human CXCR3-A and keeps the full receptor architecture, with seven membrane helices, so the calcium response transfers to it as a family inference rather than a horse assay. Horse CXCR3 GOA carries chemokine-mediated signaling pathway but no calcium-mediated signaling term, so this more specific clause is novel for the gene.
CNN. CXCR3 directs activated-lymphocyte migration, as the same human studies show. GOA already carries chemotaxis for this accession, and the curated gene review carries T cell chemotaxis, so the claim is not novel. The horse product keeps the full receptor architecture.
UNC. The investigated receptor papers do not establish this specific function for the selected horse CXCR3 product. Endothelial growth effects of a human alternative isoform are a different claim. A lineage-specific assay or mechanistic evidence is needed. PMID:12782716(https://pubmed.ncbi.nlm.nih.gov/12782716/); DOI:10.1084/jem.20021897.
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.