The selected mouse Vmn2r73 product contains the extracellular ligand-binding portion of a class C vomeronasal receptor but lacks the intact seven-transmembrane signaling module of the longer same-gene product. A signal peptide is retained. Its ligand specificity, expression as a stable protein, trafficking and possible interaction with other receptor subunits have not been established.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0004930 G protein-coupled receptor activity | IEA GO_REF:0000002 | REMOVE | Summary: The selected product lacks the intact seven-transmembrane G-protein-coupling module. Retaining the extracellular ligand-binding region does not preserve autonomous GPCR activity. This is an exact-product domain-loss argument, not a claim that the longer Vmn2r73 receptor is inactive. Supporting Evidence: file:mouse/Vmn2r73/Vmn2r73-bioinformatics/RESULTS.md | 1–429 | 1–429 | 429 | PMID:30675062 the GPCR-defining 7TM domain |
| GO:0005886 plasma membrane | IEA GO_REF:0000044 | UNDECIDED | Summary: The signal peptide supports entry into the secretory pathway, but the complete membrane-spanning receptor module is absent. Plasma-membrane retention through a partner remains possible and cannot be established from the full-length receptor annotation. Supporting Evidence: file:mouse/Vmn2r73/Vmn2r73-bioinformatics/RESULTS.md | 1–429 | 1–429 | 429 | |
| GO:0007186 G protein-coupled receptor signaling pathway | IEA GO_REF:0000002 | UNDECIDED | Summary: The fragment cannot itself execute conventional seven-transmembrane GPCR signaling, but a role as a partner, ligand-binding component or modulator has not been tested. Loss of autonomous receptor activity does not exclude every contribution to this pathway. Supporting Evidence: file:mouse/Vmn2r73/Vmn2r73-bioinformatics/RESULTS.md | 1–429 | 1–429 | 429 | PMID:30675062 the GPCR-defining 7TM domain |
| GO:0016020 membrane | IEA GO_REF:0000002 | UNDECIDED | Summary: The retained secretory signal does not establish a final compartment or stable membrane association. The normal Vmn2r73 transmembrane module is missing, while partner-mediated membrane association remains possible. Supporting Evidence: file:mouse/Vmn2r73/Vmn2r73-bioinformatics/RESULTS.md | 1–429 | 1–429 | 429 | |
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