DNA methylation plays a critical role the long-term silencing of transcription and is essential for processes such as embryonic development, germline differentiation, and tissue maturation. Dnmt3a is a member of the C5-methyltransferase family that repairs cytosines in dsDNA using a unique nucleophilic attack mechanism dependent upon the transfer of a methyl group from folate intermediates onto nucleic acids. Dnmt3a in particular performs genome-wide de novo methylation, establishes developmental DNA methylation patterns as well as paternal/maternal imprinting, and is required for methylation of most imprinted loci contained in germ cells. It can be found in both nuclear and cytoplasmic compartments and accumulates in major satellite repeats within pericentric. Canadian researchers collected compelling evidence for an essential role of Dnmt3b (but not Dnmt3a) in apoptosis of cancer cells1. The same group also published a Nature Genetics study using a Dnmt3a antibody in combination with genetic and pharmacologic inhibitors of DNA methyl transferases to better understand the role of various DNMT isotypes in oncogenic methylation2. Their studies in a wide variety of cancer cells demonstrated that Dnmt1 alone is necessary and sufficient for methylation maintenance.
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Immunocytochemistry/Immunofluorescence: Dnmt3a Antibody
A Dnmt3a antibody allowed Shen et al to profile changes in CpG island methylation during in vitro differentiation of human embryonic stem cells (ESCs), which enabled them to find abnormal methylation events occurring in a particular subset of genes which has implications for future cell transplant studies3. ChIP studies in conjunction with Dnmt3a antibody profiling allowed the creation of epigenetic silencing patterns in breast cancer cells with regards to two particular tumor suppressor genes of interest (caspase 9 and maspin)4. Stem cell research from the Whitehead Institute used a Dnmt3a antibody to characterize loss-of function induced pluripotent stem cells5. Interestingly, it was found that both Dnmt3a and Dnmt3b were dispensable in the nuclear reprogramming of somatic cells into a more pluripotent phenotype.
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