GFRA3

GFRA3
Available structures
PDBOrtholog search: PDBe RCSB
Identifiers
AliasesGFRA3, GDNFR3, GDNF family receptor alpha 3
External IDsOMIM: 605710; MGI: 1201403; HomoloGene: 1146; GeneCards: GFRA3; OMA:GFRA3 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_001496

NM_010280

RefSeq (protein)

NP_001487

NP_034410

Location (UCSC)Chr 5: 138.25 – 138.27 MbChr 18: 34.82 – 34.85 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

GDNF family receptor alpha-3 (GFRα3), also known as the artemin receptor, is a protein that in humans is encoded by the GFRA3 gene.[5][6]

Function

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The protein encoded by this gene is a glycosylphosphatidylinositol(GPI)-linked cell surface receptor and a member of the GDNF receptor family. It forms a signaling receptor complex with RET tyrosine kinase receptor and binds the artemin ligand.[6]

In mouse models of osteoarthritis, GFRα3 was upregulated in sensory nerves. Treating arthritic mice with monoclonal antibodies that bind to GFRα3 prevents artemin from binding there and signaling pain. Treated mice were able to use their limbs again two hours post-treatment.[7]

See also

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References

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  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000146013Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000024366Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ Jing S, Yu Y, Fang M, Hu Z, Holst PL, Boone T, Delaney J, Schultz H, Zhou R, Fox GM (Dec 1997). "GFRalpha-2 and GFRalpha-3 are two new receptors for ligands of the GDNF family". The Journal of Biological Chemistry. 272 (52): 33111–7. doi:10.1074/jbc.272.52.33111. PMID 9407096.
  6. ^ a b "Entrez Gene: GFRA3 GDNF family receptor alpha 3".
  7. ^ Irving, Michael (2022-01-31). ""Pain pathway" a promising new drug target to treat osteoarthritis pain". New Atlas. Retrieved 2022-02-01.

Further reading

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