Methylation and deamination of CpGs generate p53-binding sites on a genomic 
scale.

Zemojtel, Tomasz; Kielbasa, Szymon M.; Arndt, Peter F.; Chung, Ho-Ryun; Vingron, Martin

doi:10.1016/j.tig.2008.11.005

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Methylation and deamination of CpGs generate p53-binding sites on a genomic scale.

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Zemojtel, Tomasz
Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Kielbasa, Szymon M.
Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Arndt, Peter F.
Evolutionary Genomics (Peter Arndt), Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Chung, Ho-Ryun
Computational Epigenetics (Ho-Ryun Chung), Independent Junior Research Groups (OWL), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Vingron, Martin
Gene regulation (Martin Vingron), Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Citation

Zemojtel, T., Kielbasa, S. M., Arndt, P. F., Chung, H.-R., & Vingron, M. (2009). Methylation and deamination of CpGs generate p53-binding sites on a genomic scale. Trends in Genetics, 25(2), 63-66. doi:10.1016/j.tig.2008.11.005.

Cite as: https://hdl.handle.net/11858/00-001M-0000-0010-7E26-6

Abstract

The formation of transcription-factor-binding sites is an important evolutionary process. Here, we show that methylation and deamination of CpG dinucleotides generate in vivo p53-binding sites in numerous Alu elements and in non-repetitive DNA in a species-specific manner. In light of this, we propose that the deamination of methylated CpGs constitutes a universal mechanism for de novo generation of various transcription-factor-binding sites in Alus.