Selenoprotein P is a protein that in humans is encoded by the SEPP1 gene.[5][6]

SELENOP
Identifiers
AliasesSELENOP, SELP, SeP, SEPP, SEPP1, selenoprotein P, plasma, 1, selenoprotein P
External IDsOMIM: 601484; MGI: 894288; HomoloGene: 3945; GeneCards: SELENOP; OMA:SELENOP - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_005410
NM_001085486
NM_001093726

NM_001042613
NM_001042614
NM_009155

RefSeq (protein)

NP_001078955
NP_001087195
NP_005401

NP_001036078
NP_001036079
NP_033181

Location (UCSC)Chr 5: 42.8 – 42.89 MbChr 15: 3.3 – 3.31 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

This gene encodes a selenoprotein containing multiple selenocysteine (Sec) residues, which are encoded by the UGA codon that normally signals translation termination. The 3' UTR of selenoprotein 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. This selenoprotein is an extracellular glycoprotein, and is unusual in that it contains 10 Sec residues (human, rat, mouse)[7] per polypeptide, one located at the C-terminal side of protein and others at the N-terminal side. It is a heparin-binding protein that appears to be associated with endothelial cells, and has been implicated to function as an antioxidant in the extracellular space. Several transcript variants, encoding either the same or different isoform, have been found for this gene.[6]

Animal models

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Mice and dogs with knock-out variants in their SEPP1 homologues (Selenop[8] and SELENOP[9] respectively) may develop cerebellar ataxia phenotypes.[10][11] SEPP1 and neural precursor cell levels in mouse brains increase post-exercise. Mice engineered to lack SEPP1 did not increase neural precursors.[12][13]

See also

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References

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  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000250722Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000064373Ensembl, 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. ^ Hill KE, Lloyd RS, Burk RF (January 1993). "Conserved nucleotide sequences in the open reading frame and 3' untranslated region of selenoprotein P mRNA". Proceedings of the National Academy of Sciences of the United States of America. 90 (2): 537–541. Bibcode:1993PNAS...90..537H. doi:10.1073/pnas.90.2.537. PMC 45698. PMID 8421687.
  6. ^ a b "Entrez Gene: SEPP1 selenoprotein P, plasma, 1".
  7. ^ Burk and Hill 2009
  8. ^ "Selenop selenoprotein P [Mus musculus (house mouse)] - Gene - NCBI". www.ncbi.nlm.nih.gov. Retrieved 2022-01-24.
  9. ^ "SELENOP selenoprotein P [Canis lupus familiaris (dog)] - Gene - NCBI". www.ncbi.nlm.nih.gov. Retrieved 2022-01-24.
  10. ^ Christen M, Högler S, Kleiter M, Leschnik M, Weber C, Thaller D, et al. (August 2021). "Deletion of the SELENOP gene leads to CNS atrophy with cerebellar ataxia in dogs". PLOS Genetics. 17 (8): e1009716. doi:10.1371/journal.pgen.1009716. PMC 8360551. PMID 34339417.
  11. ^ Schomburg L, Schweizer U, Holtmann B, Flohé L, Sendtner M, Köhrle J (March 2003). "Gene disruption discloses role of selenoprotein P in selenium delivery to target tissues". The Biochemical Journal. 370 (Pt 2): 397–402. doi:10.1042/bj20021853. PMC 1223208. PMID 12521380.
  12. ^ PÉREZ ORTEGA R (February 3, 2022). "Widely available supplement may explain brain boost from exercise". www.science.org. Retrieved 2022-02-07.
  13. ^ Leiter O, Zhuo Z, Rust R, Wasielewska JM, Grönnert L, Kowal S, et al. (3 February 2022). "Selenium mediates exercise-induced adult neurogenesis and reverses learning deficits induced by hippocampal injury and aging". Cell Metabolism. 34 (3): 408–423.e8. doi:10.1016/j.cmet.2022.01.005. hdl:10072/418192. PMID 35120590. S2CID 246556829.

Further reading

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