ArticleBMB reports2014
Demethylation of CpG islands in the 5' upstream regions mediates the expression of the human testis-specific gene MAGEB16 and its mouse homolog Mageb16.
Article in BMB reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- MAGEB16 as an epigenetic timing regulator linking X-chromosome biology to neurodevelopmental vulnerability in Autism Spectrum Disorder.EXCLI journal · 2026Review
- Extraembryonic gut endoderm cells undergo programmed cell death during development.Nature cell biology · 2024Article
- Granulosa cell genes that regulate ovarian follicle development beyond the antral stage: The role of estrogen receptor β.Molecular and cellular endocrinology · 2021Article
- Population-specific, recent positive directional selection suggests adaptation of human male reproductive genes to different environmental conditions.BMC evolutionary biology · 2020Article
- Depletion of Mageb16 induces differentiation of pluripotent stem cells predominantly into mesodermal derivatives.Scientific reports · 2017Article
- CpG methylation differences between neurons and glia are highly conserved from mouse to human.Human molecular genetics · 2016Article
- Genome wide chromatin occupancy of mrhl RNA and its role in gene regulation in mouse spermatogonial cells.RNA biology · 2014Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
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Abstract
Tissue-specific gene expression is regulated by epigenetic modification involving trans-acting factors. Here, we identified that the human MAGEB16 gene and its mouse homolog, Mageb16, are only expressed in the testis. To investigate the mechanism governing their expression, the promoter methylation status of these genes was examined in different samples. Two CpG islands (CGIs) in the 5' upstream region of MAGEB16 were highly demethylated in human testes, whereas they were methylated in cells without MAGEB16 expression. Similarly, the CGI in Mageb16 was hypomethylated in mouse testes but hypermethylated in other tissues and cells without Mageb16 expression. Additionally, the expression of these genes could be activated by treatment with the demethylation agent 5'-aza-2'-deoxycytidine (5'-aza-CdR). Luciferase assays revealed that both gene promoter activities were inhibited by methylation of the CGI regions. Therefore, we propose that the testis-specific expression of MAGEB16 and Mageb16 is regulated by the methylation status of their promoter regions.
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