CXCR3 is a seven-transmembrane chemokine receptor that recognizes CXCL9, CXCL10 and CXCL11 and coordinates lymphocyte recruitment through G-protein signaling. Human alternative isoforms differ in ligand recognition and downstream growth responses; CXCR3-B also recognizes CXCL4 and mediates angiostatic responses.
CXCR3-A and CXCR3-B share the seven-transmembrane receptor core but differ at the N terminus and in signaling behavior. In the directly inspected Lasagni study, CXCR3-A supports cell survival/proliferation, whereas CXCR3-B supports endothelial growth inhibition and apoptosis; CXCL4 preferentially binds the B isoform. The paper explicitly includes a negative competition panel containing CCL3, CCL4 and CCL5/RANTES. That experiment is decisive against treating the named ligand list in the horse model output as established. It does not prove that every conceivable CC ligand fails to interact with every CXCR3 isoform. The C-C receptor/binding IBA annotations require tracing the curated ancestral claim and its actual experimental grounding, not counting donor proteins.
From PMID:12782716(https://pubmed.ncbi.nlm.nih.gov/12782716/):
Human microvascular endothelial cell line-1 (HMEC-1), transfected with either the known CXCR3 (renamed CXCR3-A) or CXCR3-B, bound CXCL9, CXCL10, and CXCL11, whereas CXCL4 showed high affinity only for CXCR3-B.
The exact target is A0A9L0T1D1, not an arbitrary horse record with a matching name. The reproducible paired-sequence analysis records identity, coverage and internal gaps. It supports homology but is not a reciprocal orthology test. Molecular properties are transferred only with the relevant domain, targeting and paralog constraints. The prediction-time sequence is not independently verified.
The following annotation scopes need source-specific follow-up: C-C chemokine binding, C-C chemokine receptor activity, cell adhesion, cytoplasm, protein binding, regulation of cell adhesion, signaling receptor activity. Experimental annotations are not removed merely because a cached abstract omits the gene or a specific assay. High-throughput protein-binding rows require their actual partner or complex context before replacement with an informative molecular function.
Research provenance: external Falcon/Edison was attempted with Perplexity fallback. Some requests returned HTTP 429 and fallback returned insufficient-quota HTTP 401; successful external reports are preserved separately. Primary-source manual synthesis is explicitly labeled manual where no external report was available.