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DNA (cytosine-5)-methyltransferase 1 (DNMT1) and its paralogs DNMT3A and DNMT3B are enzymes that catalyze the transfer of methyl groups to cytosine residues in DNA, predominantly at CpG dinucleotides, resulting in DNA methylation[1][2][3]. DNMT1 is primarily responsible for maintenance methylation after DNA replication, ensuring the faithful inheritance of epigenetic marks, while DNMT3A and DNMT3B are primarily involved in de novo DNA methylation during development[1][3]. Aberrant activity or expression of these enzymes is implicated in various human disorders, most notably cancer, where altered methylation patterns can lead to inappropriate gene silencing[2][3]. Drugs targeting DNMTs, such as azacitidine and decitabine, are used in the treatment of certain leukemias and myelodysplastic syndromes, working by inhibiting DNMT activity and thereby reversing abnormal gene silencing[2][3]. DNMT1, DNMT3A, and DNMT3B are major regulators of epigenetic programming and play essential roles in cellular differentiation, genomic imprinting, X-chromosome inactivation, and suppression of transposable elements[1][2][3].
Inhibition of DNA methyltransferase activity, leading to DNA hypomethylation and reactivation of silenced tumor suppressor genes
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