Glutathione peroxidase 6
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(Redirected from GPX6)
Protein-coding gene in the species Homo sapiens
| GPX6 | |||||||||||||||||||||||||||||||||||||||||||||||
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| Aliases | GPX6 , GPX5p, GPXP3, GPx-6, GSHPx-6, dJ1186N24, dJ1186N24.1, glutathione peroxidase 6 | ||||||||||||||||||||||||||||||||||||||||||||||
| External IDs | OMIM: 607913; MGI: 1922762; HomoloGene: 130008; GeneCards: GPX6; OMA:GPX6 - orthologs | ||||||||||||||||||||||||||||||||||||||||||||||
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Glutathione peroxidase 6 (GPx-6) is an enzyme that in humans is encoded by the GPX6 gene.[5] [6]
This gene product belongs to the glutathione peroxidase family, which functions in the detoxification of hydrogen peroxide. It contains a selenocysteine (Sec) residue at its active site. The selenocysteine is encoded by the UGA codon, which normally signals translation termination. The 3' UTR of Sec-containing genes have a common stem-loop structure, the sec insertion sequence (SECIS), which is necessary for the recognition of UGA as a Sec codon rather than as a stop signal. Expression of this gene is restricted to embryos and adult olfactory epithelium.[5]
References
[edit ]- ^ a b c ENSG00000198704 GRCh38: Ensembl release 89: ENSG00000281185, ENSG00000198704 – Ensembl, May 2017
- ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000004341 – Ensembl, May 2017
- ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
- ^ a b "Entrez Gene: glutathione peroxidase 6 (olfactory)".
- ^ Kryukov GV, Castellano S, Novoselov SV, Lobanov AV, Zehtab O, Guigó R, Gladyshev VN (May 2003). "Characterization of mammalian selenoproteomes". Science. 300 (5624): 1439–43. Bibcode:2003Sci...300.1439K. doi:10.1126/science.1083516. PMID 12775843. S2CID 10363908.
Further reading
[edit ]- Talmud PJ, Drenos F, Shah S, et al. (2009). "Gene-centric association signals for lipids and apolipoproteins identified via the HumanCVD BeadChip". Am. J. Hum. Genet. 85 (5): 628–42. doi:10.1016/j.ajhg.2009年10月01日4. PMC 2775832 . PMID 19913121.
- Richard MJ, Guiraud P, Didier C, et al. (2001). "Human immunodeficiency virus type 1 Tat protein impairs selenoglutathione peroxidase expression and activity by a mechanism independent of cellular selenium uptake: consequences on cellular resistance to UV-A radiation". Arch. Biochem. Biophys. 386 (2): 213–20. doi:10.1006/abbi.2000.2197. PMID 11368344.
- Opalenik SR, Ding Q, Mallery SR, Thompson JA (1998). "Glutathione depletion associated with the HIV-1 TAT protein mediates the extracellular appearance of acidic fibroblast growth factor". Arch. Biochem. Biophys. 351 (1): 17–26. doi:10.1006/abbi.1997.0566. PMID 9501919.
- Choi J, Liu RM, Kundu RK, et al. (2000). "Molecular mechanism of decreased glutathione content in human immunodeficiency virus type 1 Tat-transgenic mice". J. Biol. Chem. 275 (5): 3693–8. doi:10.1074/jbc.275.5.3693 . PMID 10652368.
- Strausberg RL, Feingold EA, Grouse LH, et al. (2002). "Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences". Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899–903. Bibcode:2002PNAS...9916899M. doi:10.1073/pnas.242603899 . PMC 139241 . PMID 12477932.
- Price TO, Ercal N, Nakaoke R, Banks WA (2005). "HIV-1 viral proteins gp120 and Tat induce oxidative stress in brain endothelial cells". Brain Res. 1045 (1–2): 57–63. doi:10.1016/j.brainres.2005年03月03日1. PMID 15910762. S2CID 7362454.
- Bailey SD, Xie C, Do R, et al. (2010). "Variation at the NFATC2 locus increases the risk of thiazolidinedione-induced edema in the Diabetes REduction Assessment with ramipril and rosiglitazone Medication (DREAM) study". Diabetes Care. 33 (10): 2250–3. doi:10.2337/dc10-0452. PMC 2945168 . PMID 20628086.
- Moyer AM, Sun Z, Batzler AJ, et al. (2010). "Glutathione pathway genetic polymorphisms and lung cancer survival after platinum-based chemotherapy". Cancer Epidemiol. Biomarkers Prev. 19 (3): 811–21. doi:10.1158/1055-9965.EPI-09-0871. PMC 2837367 . PMID 20200426.
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