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Devos J, Weselake SV, Wevrick R. Magel2, a Prader-Willi syndrome candidate gene, modulates the activities of circadian rhythm proteins in cultured cells. J Circadian Rhythms. 2011;9(1):12doi: 10.1186/1740-3391-9-12.
Devos, J., Weselake, S. V., & Wevrick, R. (2011). Magel2, a Prader-Willi syndrome candidate gene, modulates the activities of circadian rhythm proteins in cultured cells. Journal of circadian rhythms, 9(1), 12. https://doi.org/10.1186/1740-3391-9-12
Devos, Julia, et al. "Magel2, a Prader-Willi syndrome candidate gene, modulates the activities of circadian rhythm proteins in cultured cells." Journal of circadian rhythms vol. 9,1 (2011): 12. doi: https://doi.org/10.1186/1740-3391-9-12
Devos J, Weselake SV, Wevrick R. Magel2, a Prader-Willi syndrome candidate gene, modulates the activities of circadian rhythm proteins in cultured cells. J Circadian Rhythms. 2011 Dec 30;9(1):12. doi: 10.1186/1740-3391-9-12. PMID: 22208286; PMCID: PMC3278377.
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J Circadian Rhythms. 2011 Dec 30;9(1):12. doi: 10.1186/1740-3391-9-12.

Magel2, a Prader-Willi syndrome candidate gene, modulates the activities of circadian rhythm proteins in cultured cells.

Journal of circadian rhythms

Julia Devos, Sara V Weselake, Rachel Wevrick

Affiliations

  1. Department of Medical Genetics, University of Alberta, Edmonton, AB Canada T6G 2H7. [email protected].

PMID: 22208286 PMCID: PMC3278377 DOI: 10.1186/1740-3391-9-12

Abstract

BACKGROUND: The Magel2 gene is most highly expressed in the suprachiasmatic nucleus of the hypothalamus, where its expression cycles in a circadian pattern comparable to that of clock-controlled genes. Mice lacking the Magel2 gene have hypothalamic dysfunction, including circadian defects that include reduced and fragmented total activity, excessive activity during the subjective day, but they have a normal circadian period. Magel2 is a member of the MAGE family of proteins that have various roles in cellular function, but the specific function of Magel2 is unknown.

METHODS: We used a variety of cell-based assays to determine whether Magel2 modifies the properties of core circadian rhythm proteins.

RESULTS: Magel2 represses the activity of the Clock:Bmal1 heterodimer in a Per2-luciferase assay. Magel2 interacts with Bmal1 and with Per2 as measured by co-immunoprecipitation in co-transfected cells, and exhibits a subcellular distribution consistent with these interactions when visualized by immunofluorescence. As well, Magel2 induces the redistribution of the subcellular localization of Clock towards the cytoplasm, in contrast to the nucleus-directed effect of Bmal1 on Clock subcellular localization.

CONCLUSION: Consistent with the blunted circadian rhythm observed in Magel2-null mice, these data suggest that Magel2 normally promotes negative feedback regulation of the cellular circadian cycle, through interactions with key core circadian rhythm proteins.

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