ArticleThe Journal of biological chemistry2010
The inherent processivity of the human de novo methyltransferase 3A (DNMT3A) is enhanced by DNMT3L.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 95 citations in OpenAlex.
- Mechanisms of DNA methyltransferase 3A1-mediated DNA methylation of nucleosomes.The Journal of biological chemistry · 2026Article
- RECAP-seq: restriction enzyme-based CpG-methylated fragment amplification for early cancer detection.Scientific reports · 2025Article
- Non-canonical functions of DNMT3A in hematopoietic stem cells regulate telomerase activity and genome integrity.Cell stem cell · 2025Article
- Mechanism of non-coding RNA regulation of DNMT3A.Epigenetics & chromatin · 2025Article
- Rescuing DNMT1 fails to fully reverse the molecular and functional repercussions of its loss in mouse embryonic stem cells.Nucleic acids research · 2025Article
- Enzymology of Mammalian DNA Methyltransferases.Advances in experimental medicine and biology · 2022Article
- Neuronal activation modulates enhancer activity of genes for excitatory synaptogenesis through de novo DNA methylation.The Journal of reproduction and development · 2021Article
- Discovering candidate imprinted genes and imprinting control regions in the human genome.BMC genomics · 2020Article
- Structural insights into CpG-specific DNA methylation by human DNA methyltransferase 3B.Nucleic acids research · 2020Article
- The R882H substitution in the humanThe Journal of biological chemistry · 2019Article
- The R882H DNMT3A hot spot mutation stabilizes the formation of large DNMT3A oligomers with low DNA methyltransferase activity.The Journal of biological chemistry · 2019Article
- Article
- A Model System for Studying the DNMT3A Hotspot Mutation (DNMT3ACancer research · 2019Article
- Mutations in the DNMT3A DNA methyltransferase in acute myeloid leukemia patients cause both loss and gain of function and differential regulation by protein partners.The Journal of biological chemistry · 2019Article
- The DNMT3A R882H mutation does not cause dominant negative effects in purified mixed DNMT3A/R882H complexes.Scientific reports · 2018Article
- Dnmt3b Methylates DNA by a Noncooperative Mechanism, and Its Activity Is Unaffected by Manipulations at the Predicted Dimer Interface.Biochemistry · 2018Article
- Precise Epigenome Editing on the Stage: A Novel Approach to Modulate Gene Expression.Epigenetics insights · 2018Article
- DNA epigenome editing using CRISPR-Cas SunTag-directed DNMT3A.Genome biology · 2017Article
- Differential landscape of non-CpG methylation in embryonic stem cells and neurons caused by DNMT3s.Scientific reports · 2017Article
- rahu is a mutant allele of Dnmt3c, encoding a DNA methyltransferase homolog required for meiosis and transposon repression in the mouse male germline.PLoS genetics · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human DNMT3A is responsible for de novo DNA cytosine methylation patterning during development. Here we show that DNMT3A methylates 5-8 CpG sites on human promoters before 50% of the initially bound enzyme dissociates from the DNA. Processive methylation is enhanced 3-fold in the presence of DNMT3L, an inactive homolog of DNMT3A, therefore providing a mechanism for the previously described DNMT3L activation of DNMT3A. DNMT3A processivity on human promoters is also regulated by DNA topology, where a 2-fold decrease in processivity was observed on supercoiled DNA in comparison with linear DNA. These results are the first observation that DNMT3A utilizes this mechanism of increasing catalytic efficiency. Processive de novo DNA methylation provides a mechanism that ensures that multiple CpG sites undergo methylation for transcriptional regulation and silencing of newly integrated viral DNA.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.