Title |
H3K4me3 inversely correlates with DNA methylation at a large class of non-CpG-island containing start sites
|
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Published in |
Genome Medicine, May 2012
|
DOI | 10.1186/gm346 |
Pubmed ID | |
Authors |
Dheepa Balasubramanian, Batool Akhtar-Zaidi, Lingyun Song, Cynthia F Bartels, Martina Veigl, Lydia Beard, Lois Myeroff, Kishore Guda, James Lutterbaugh, Joseph Willis, Gregory E Crawford, Sanford D Markowitz, Peter C Scacheri, Balasubramanian D, Akhtar-Zaidi B, Song L, Bartels CF, Veigl M, Beard L, Myeroff L, Guda K, Lutterbaugh J, Willis J, Crawford GE, Markowitz SD, Scacheri PC |
Abstract |
In addition to mutations, epigenetic silencing of genes has been recognized as a fundamental mechanism that promotes human carcinogenesis. To date, characterization of epigenetic gene silencing has largely focused on genes in which silencing is mediated by hypermethylation of promoter-associated CpG islands, associated with loss of the H3K4me3 chromatin mark. Far less is known about promoters lacking CpG-islands or genes that are repressed by alternative mechanisms. |
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