期刊
PLOS ONE
卷 3, 期 9, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0003294
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资金
- European Union [LSHG-CT-2006-018739]
- Spanish Ramon & Cajal Programme
- Health Department of the Spanish Government [PI061267, PI051707]
- Health and Education and Science Departments of the Spanish Government [FIS01-04, MCYT08-03, FU2004-02073, MEC09-05]
- TRANSFOG [LSHC-CT-2004-503438]
- Spanish Association Against Cancer (AECC)
- FPU Spanish Research Programme [Fellowship]
- Consejeria de Salud de la Junta de Andalucia [0029, 0030/2006]
- Spanish Ministry of Health [FIS PI070026]
- International Jose Carreras Foundation against Leukemia [EDThomas-05]
- ISCIII
- DFG
- Hertie Foundation
- Fundacion Progreso y Salud
- Instituto de Salud Carlos III-Red Espanola de Terapia Celular [RD06/0010/0025]
- MRC
- MRC [G0801059, G0700785, G0300268] Funding Source: UKRI
- Medical Research Council [G0700785, G0801059, G0300268] Funding Source: researchfish
Developmental genes are silenced in embryonic stem cells by a bivalent histone-based chromatin mark. It has been proposed that this mark also confers a predisposition to aberrant DNA promoter hypermethylation of tumor suppressor genes (TSGs) in cancer. We report here that silencing of a significant proportion of these TSGs in human embryonic and adult stem cells is associated with promoter DNA hypermethylation. Our results indicate a role for DNA methylation in the control of gene expression in human stem cells and suggest that, for genes repressed by promoter hypermethylation in stem cells in vivo, the aberrant process in cancer could be understood as a defect in establishing an unmethylated promoter during differentiation, rather than as an anomalous process of de novo hypermethylation.
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