MAGED1

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Template:Cs1 config Template:Short description An Error has occurred retrieving Wikidata item for infobox Melanoma-associated antigen D1 is a protein that in humans is encoded by the MAGED1 gene.[1][2]

Function

This gene is a member of the melanoma antigen gene (MAGE) family. Most of the genes of this family encode tumor specific antigens that are not expressed in normal adult tissues except testis. Although the protein encoded by this gene shares strong homology with members of the MAGE family, it is expressed in almost all normal adult tissues. This gene has been demonstrated to be involved in the p75 neurotrophin receptor mediated programmed cell death pathway. Three transcript variants encoding two different isoforms have been found for this gene.[2]

MAGED was found to be deleted in a group of children with an intellectual disability disorder caused by a Xp11.22 deletion.[3]

Maged1 plays a role in controlling the reward circuitry in the brain of mice that is responsible for addictive behaviors.[4] More recently, it has been shown to play a role in drug addiction through an epigenetic mechanism involving the monoubiquitination of H2A, which represses gene expression via interaction with the deubiquitinase USP7.[5]

Interactions

MAGED1 has been shown to interact with UNC5A,[6] PJA1,[7] XIAP,[8] and USP7.[5]

References

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  1. ^ Page Module:Citation/CS1/styles.css has no content.Põld M, Zhou J, Chen GL, Hall JM, Vescio RA, Berenson JR (Sep 1999). "Identification of a new, unorthodox member of the MAGE gene family". Genomics. 59 (2): 161–7. doi:10.1006/geno.1999.5870. PMID 10409427.
  2. ^ a b Page Module:Citation/CS1/styles.css has no content."Entrez Gene: MAGED1 melanoma antigen family D, 1".
  3. ^ Page Module:Citation/CS1/styles.css has no content.Grau C, Starkovich M, Azamian MS, Xia F, Cheung SW, Evans P, et al. (2017). "Xp11.22 deletions encompassing CENPVL1, CENPVL2, MAGED1 and GSPT2 as a cause of syndromic X-linked intellectual disability". PLOS ONE. 12 (4) e0175962. Bibcode:2017PLoSO..1275962G. doi:10.1371/journal.pone.0175962. PMC 5393878. PMID 28414775.
  4. ^ Page Module:Citation/CS1/styles.css has no content.De Backer JF, Monlezun S, Detraux B, Gazan A, Vanopdenbosch L, Cheron J, et al. (July 2018). "Deletion of Maged1 in mice abolishes locomotor and reinforcing effects of cocaine". EMBO Reports. 19 (9) e45089. doi:10.15252/embr.201745089. PMC 6123657. PMID 30002119.*Template:Lay source
  5. ^ a b Page Module:Citation/CS1/styles.css has no content.Cheron J, Beccari L, Hagué P, Icick R, Despontin C, Carusone T, et al. (December 2023). "USP7/Maged1-mediated H2A monoubiquitination in the paraventricular thalamus: an epigenetic mechanism involved in cocaine use disorder". Nature Communications. 14 (1) 8481. Bibcode:2023NatCo..14.8481C. doi:10.1038/s41467-023-44120-2. PMC 10733359. PMID 38123574.
  6. ^ Page Module:Citation/CS1/styles.css has no content.Williams ME, Strickland P, Watanabe K, Hinck L (May 2003). "UNC5H1 induces apoptosis via its juxtamembrane region through an interaction with NRAGE". J. Biol. Chem. 278 (19): 17483–90. doi:10.1074/jbc.M300415200. PMID 12598531.
  7. ^ Page Module:Citation/CS1/styles.css has no content.Sasaki A, Masuda Y, Iwai K, Ikeda K, Watanabe K (Jun 2002). "A RING finger protein Praja1 regulates Dlx5-dependent transcription through its ubiquitin ligase activity for the Dlx/Msx-interacting MAGE/Necdin family protein, Dlxin-1". J. Biol. Chem. 277 (25): 22541–6. doi:10.1074/jbc.M109728200. PMID 11959851.
  8. ^ Page Module:Citation/CS1/styles.css has no content.Jordan BW, Dinev D, LeMellay V, Troppmair J, Gotz R, Wixler L, et al. (Oct 2001). "Neurotrophin receptor-interacting mage homologue is an inducible inhibitor of apoptosis protein-interacting protein that augments cell death". J. Biol. Chem. 276 (43): 39985–9. doi:10.1074/jbc.C100171200. PMID 11546791.

Further reading

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