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DNA methylation is a fundamental epigenetic modification involving the addition of a methyl group to the 5-carbon position of cytosine residues in DNA, catalyzed by DNA methyltransferase enzymes such as DNMT1, DNMT3A, and DNMT3B[1][3][5][6][8]. Methylation predominantly occurs at CpG dinucleotides and can stably repress gene transcription, influence chromatin structure, and direct cell differentiation and tissue-specific gene expression[1][3][6]. These processes are reversible by enzymes in the TET family that oxidize methylcytosine, and are crucial for biological functions such as imprinting, embryonic development, and maintenance of genome stability[1][4][8]. Aberrant DNA methylation is implicated in a wide range of diseases, including cancers, by silencing tumor suppressor genes, as well as neurodegenerative and developmental disorders[1][7]. Although drugs target the enzymes mediating methylation, "DNA methylation processes" themselves are not considered a single canonical therapeutic target, but rather a critical pathway and analytical biomarker in translational medicine[7][10]. This entry is not a specific molecule, receptor, or therapeutic target but refers to a set of dynamic enzymatic processes essential for epigenetic regulation. For structured data, individual components such as "DNA methyltransferase 1 (DNMT1)," "DNA methyltransferase 3A (DNMT3A)," or "Ten-eleven translocation methylcytosine dioxygenase (TET)" should be considered as specific molecular targets.
Inhibition of DNA methyltransferase enzymes (DNMT inhibitors block methyl group transfer to DNA)[7][5]
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