Oxidative damage to methyl-CpG sequences inhibits the binding of the methyl-CpG binding domain (MBD) of methyl-CpG binding protein 2 (MeCP2).

By Victoria Valinluck, Hsin-hao Tsai, Daniel K. Rogstad, A. Burdzy, A. Bird, L. Sowers. Nucleic Acids Research, 2004

799 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/523e61148ef4eef227cb2e03c025bf80c74b0862

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In Genetics

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Citations in the corpus

• Base-Resolution Analysis of 5-Hydroxymethylcytosine in the Mammalian Genome (2012, positive): “Similarly, it has been suggested that 5hmC offers a different platform upon which transcription factors may bind or 5mC specific binding proteins may be excluded (Hashimoto et al., 2012; Kriaucionis and Heintz, 2009; Valinluck et al., 2004; Yildirim et al., 2011).”
• Rapid DNA methylation changes after exposure to traffic particles. (2009, background): “Winter 192 (18) 125 (17) 54 (15) 13 (45)”
• Reversing DNA Methylation: Mechanisms, Genomics, and Biological Functions (2014, positive): “…hemihydroxymethylated CpG sites (hCG:GC) (Frauer et al., 2011; Hashimoto et al., 2012), independent studies have established that DNMT1 is significantly less efficient (10 60- fold) in methylating hCG:GC than hemimethylated (mCG:GC) sites in vitro (Hashimoto et al., 2012; Valinluck et al., 2004).”
• Mechanisms and functions of Tet protein-mediated 5-methylcytosine oxidation. (2011, background): “Indeed, MBD-containing proteins such as methyl-CpG-binding protein 2 (MeCP2) 2440 GENES & DEVELOPMENT do not recognize 5hmC (Valinluck et al. 2004; Jin et al. 2010), thereby providing a potential means to reverse the gene silencing effect mediated by promoter DNA methylation-dependent recruitment…”
• Tissue Distribution of 5-Hydroxymethylcytosine and Search for Active Demethylation Intermediates (2010, background): “For example it was shown that methyl-CpG binding protein 2 (MeCP2) no longer binds to the corresponding sequences when mCs were converted to hmCs in CpG sequences [13].”
• DNA Methylation and Its Basic Function (2013, background): “In support of this theory, the conversion of 5mC to 5hmC impairs the binding of the repressive methyl-binding protein MeCP2 (Valinluck et al, 2004).”
• Changes in DNA methylation patterns in subjects exposed to low-dose benzene. (2007, background): “In addition, reactive oxygen species and oxidative DNA damage produced by benzene may reduce binding affinity of the methyl-CpG binding protein 2, thereby resulting in epigenetic alterations (18).”
• Oxidative stress and diabetic retinopathy: Molecular mechanisms, pathogenetic role and therapeutic implications (2020, background): “Oxidative-damaged methyl-CpG sequences bring about epigenetic alterations in chromatin organization through the blockage of the binding between the methyl-CpG site and the binding domain of methyl-CpG binding protein 2 (MeCP2) [101], contributing to”
• Oxidative stress, DNA methylation and carcinogenesis. (2008, background): “Incorporation of 8-OHdG and 5-hydroxymethylcytosine (the oxidation by-product of 5- methylcytosine) in the MBP recognition sequence resulted in the significant inhibition of the binding affinity of MBP [46].”
• Uncovering the role of 5-hydroxymethylcytosine in the epigenome (2011, background): “Other than its potential involvement in demethylation, the presence of 5hmC may relieve the silencing effect of 5mC by preventing binding of methyl-binding protein”
• The Behaviour of 5-Hydroxymethylcytosine in Bisulfite Sequencing (2010, background): “This indicates that sites of hydroxymethylation would likely appear methylated by bisulfite sequencing but unmethylated by detection techniques that rely on antibody [14,16].”
• MeCP2 binds to 5hmc enriched within active genes and accessible chromatin in the nervous system (2013, neutral): “The identification of MeCP2 as a major 5hmC binding protein in rodent brain is surprising given previous in vitro studies reporting that it binds 5mC containing DNA much more avidly than 5hmC containing DNA (Bostick et al., 2007; Valinluck et al., 2004).”