SLC2A9

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Identifiers
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External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez
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Solute carrier family 2, facilitated glucose transporter member 9 is a protein that in humans is encoded by the SLC2A9 gene.[1][2][3]

This gene encodes a member of the SLC2A facilitative glucose transporter family. Members of this family play a significant role in maintaining glucose homeostasis. The encoded protein may play a role in the development and survival of chondrocytes in cartilage matrices. Two transcript variants encoding distinct isoforms have been identified for this gene.[3]

SLC2A9 has also recently been found to transport uric acid, and genetic variants of the transporter have been linked to increased risk of development of both hyperuricemia, gout and Alzheimer's disease.[4][5][6]

See also

References

  1. Phay JE, Hussain HB, Moley JF (Aug 2000). "Cloning and expression analysis of a novel member of the facilitative glucose transporter family, SLC2A9 (GLUT9)". Genomics. 66 (2): 217–20. doi:10.1006/geno.2000.6195. PMID 10860667.
  2. Manolescu AR, Augustin R, Moley K, Cheeseman C (Aug 2007). "A highly conserved hydrophobic motif in the exofacial vestibule of fructose transporting SLC2A proteins acts as a critical determinant of their substrate selectivity". Mol Membr Biol. 24 (5–6): 455–63. doi:10.1080/09687680701298143. PMID 17710649.
  3. 3.0 3.1 "Entrez Gene: SLC2A9 solute carrier family 2 (facilitated glucose transporter), member 9".
  4. Vitart V, Rudan I, Hayward C, et al. (2008). "SLC2A9 is a newly identified urate transporter influencing serum urate concentration, urate excretion and gout". Nature Genetics. 40 (4): 437–42. doi:10.1038/ng.106. PMID 18327257.
  5. Döring A, Gieger C, Mehta D, et al. (2008). "SLC2A9 influences uric acid concentrations with pronounced sex-specific effects". Nature Genetics. 40 (4): 430–6. doi:10.1038/ng.107. PMID 18327256.
  6. Hollingworth P, Sweet R, Sims R, et al. (2012). "Genome-wide association study of Alzheimer's disease with psychotic symptoms". Molecular Psychiatry. 17: 1316–1327. doi:10.1038/mp.2011.125.

Further reading

This article incorporates text from the United States National Library of Medicine, which is in the public domain.



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