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• W2064084554 startingPage "374" @default.
• W2064084554 abstract "In recent years, epigenetic alterations have come to prominence in cancer research. In particular, hypermethylation of CpG islands located in the promoter regions of tumor-suppressor genes is now firmly established as an important mechanism for gene inactivation in cancer. One of the most remarkable achievements in the field has been the identification of the methyl-CpG-binding domain family of proteins, which provide mechanistic links between specific patterns of DNA methylation and histone modifications. Although many of the current data indicate that methyl-CpG-binding proteins play a key role in maintaining a transcriptionally inactive state of methylated genes, MBD4 is also known to be involved in excision repair of T:G mismatches. The latter is a member of this family of proteins and appears to play a role in reducing mutations at 5-methylcytosine. This review examines the contribution of methyl-CpG-binding proteins in the epigenetic pathway of cancer.Key words: methyl-CpG-binding, MeCP2, DNA methylation, Rett syndrome, cancer epigenetics." @default.
• W2064084554 created "2016-06-24" @default.
• W2064084554 creator A5010137759 @default.
• W2064084554 creator A5082124562 @default.
• W2064084554 date "2005-06-01" @default.
• W2064084554 modified "2023-10-10" @default.
• W2064084554 title "Methyl-CpG-binding proteins in cancer: blaming the DNA methylation messenger" @default.
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• W2064084554 doi "https://doi.org/10.1139/o05-035" @default.
• W2064084554 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15959563" @default.

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