DNA methylation is a crucial epigenetic modification that plays a pivotal role in regulating gene expression and maintaining genome stability in various organisms. DNA methyltransferases (DNMTs) are the enzymes responsible for adding a methyl group (-CH3) to the cytosine base of DNA, primarily at CpG dinucleotides. These DNMTs are integral to the process of DNA methylation and are essential for numerous biological processes. DNMTs belong to a family of enzymes that includes three primary members in mammals: DNMT1, DNMT3A, and DNMT3B, with each of these enzymes having distinct roles in DNA methylation. DNMT1 is often referred to as the maintenance methyltransferase because it primarily functions to maintain an existing DNA methylation pattern during DNA replication. It recognizes hemi-methylated CpG sites (where only one DNA strand is methylated) and adds a methyl group to the unmethylated cytosine on the newly synthesized DNA strand. This ensures that the methylation pattern is faithfully propagated to both daughter cells during cell division. DNMT3A and DNMT3B are known as de novo methyltransferases because they primarily initiate DNA methylation by adding methyl groups to previously unmethylated CpG sites. They therefore play a crucial role in establishing new methylation patterns during early development and during tissue-specific differentiation. Mutations in these enzymes are therefore associated with some genetic disorders, including Tatton-Brown-Rahman Syndrome (TBRS), characterized by overgrowth and intellectual disability, and caused by mutations in either DNMT3A or DNMT3B. DNMTs are responsible for establishing and maintaining DNA methylation patterns which are tissue-specific, varying significantly between cell types. These patterns are critical for gene regulation, as methylation at promoter regions typically represses gene transcription, whilst methylation within genes can enhance transcription. DNA methylation is a key player in epigenetic regulation, influencing gene expression without altering the underlying DNA sequence. DNMTs help regulate this, thereby controlling various biological processes including embryonic development, X-chromosome inactivation, and cellular differentiation. Dysregulation of DNMT activity can lead to aberrant DNA methylation patterns, which are often associated with diseases such as cancer. In cancer, hypomethylation (reduced methylation) at CpG islands in gene promoters can lead for example to the overexpression of oncogenes, whilst hypermethylation can silence tumour suppressor genes, contributing to cancer development. DNMTs can also be influenced by environmental factors such as diet, exposure to toxins, and lifestyle choices. These factors can lead to changes in DNA methylation patterns and contribute to the development of various diseases, including metabolic disorders and neurodegenerative diseases. For example, folate, a B-vitamin, is particularly important for DNA methylation. It is involved in the synthesis of methionine, which is a precursor of S-adenosylmethionine (SAM), a key cofactor for DNMTs. Low dietary intake of folate can therefore lead to DNA hypomethylation, potentially impacting gene expression and epigenetic regulation. Given their roles in gene regulation and disease development, DNMTs have emerged as potential therapeutic targets. DNMT inhibitors, such as 5-azacytidine and decitabine, have been developed to modulate DNA methylation patterns and are used in the treatment of certain cancers, particularly myelodysplastic syndromes (MDS) and acute myeloid leukaemia (AML). We offer a wide product range of research reagents for studying DNMTs, including Dnmt1 antibodies, MGMT antibodies, Dnmt3b antibodies, and Dnmt3a antibodies. Explore our full DNMTs product range below and discover more, for less.