ArticlePloS one2013
Inactive DNMT3B splice variants modulate de novo DNA methylation.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 66 citations in OpenAlex.
- Multidomain interaction governs the filamentous assembly of the dominant-negative DNMT3A R882H mutant.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Chromatin binding and N-terminal domains of DNMT3B1 confer specificity for developmentally regulated CpG island methylation.Genes & development · 2026Article
- Nucleosome spacing regulates linker methylation by DNMT3A2/3B3.Molecular cell · 2026Article
- Catalytic-independent roles of chromatin modifiers in mammalian development and the implications for treating human disease.Biochemical Society transactions · 2025Review
- Using human disease mutations to understand de novo DNA methyltransferase function.Biochemical Society transactions · 2024Review
- Epigenetic control of skeletal muscle atrophy.Cellular & molecular biology letters · 2024Review
- Effect of Withaferin-A, Withanone, and Caffeic Acid Phenethyl Ester on DNA Methyltransferases: Potential in Epigenetic Cancer Therapy.Current topics in medicinal chemistry · 2024Article
- Expression of DNA Methyltransferase 3B Isoforms Is Associated with DNA Satellite 2 Hypomethylation and Clinical Prognosis in Advanced High-Grade Serous Ovarian Carcinoma.International journal of molecular sciences · 2022Article
- Genomic targets and selective inhibition of DNA methyltransferase isoforms.Clinical epigenetics · 2022Article
- DNA Methyltransferases: From Evolution to Clinical Applications.International journal of molecular sciences · 2022Review
- Definition of germ layer cell lineage alternative splicing programs reveals a critical role for Quaking in specifying cardiac cell fate.Nucleic acids research · 2022Article
- Targeting DNMTs to Overcome Enzalutamide Resistance in Prostate Cancer.Molecular cancer therapeutics · 2022Article
- Aberrant DNA methylation in multiple myeloma: A major obstacle or an opportunity?Frontiers in oncology · 2022Review
- Epigenetic Characteristics of Human Subtelomeres Vary in Cells Utilizing the Alternative Lengthening of Telomeres (ALT) Pathway.Life (Basel, Switzerland) · 2021Article
- Epigenetic dynamics in cancer stem cell dormancy.Cancer metastasis reviews · 2020Review
- TETs compete with DNMT3 activity in pluripotent cells at thousands of methylated somatic enhancers.Nature genetics · 2020Article
- A Functional Kinase Is Necessary for Cyclin-Dependent Kinase G1 (CDKG1) to Maintain Fertility at High Ambient Temperature inFrontiers in plant science · 2020Article
- DNMT3B shapes the mCA landscape and regulates mCG for promoter bivalency in human embryonic stem cells.Nucleic acids research · 2019Article
- A Model System for Studying the DNMT3A Hotspot Mutation (DNMT3ACancer research · 2019Article
- Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inactive DNA methyltransferase (DNMT) 3B splice isoforms are associated with changes in DNA methylation, yet the mechanisms by which they act remain largely unknown. Using biochemical and cell culture assays, we show here that the inactive DNMT3B3 and DNMT3B4 isoforms bind to and regulate the activity of catalytically competent DNMT3A or DNMT3B molecules. DNMT3B3 modestly stimulated the de novo methylation activity of DNMT3A and also counteracted the stimulatory effects of DNMT3L, therefore leading to subtle and contrasting effects on activity. DNMT3B4, by contrast, significantly inhibited de novo DNA methylation by active DNMT3 molecules, most likely due to its ability to reduce the DNA binding affinity of co-complexes, thereby sequestering them away from their substrate. Immunocytochemistry experiments revealed that in addition to their effects on the intrinsic catalytic function of active DNMT3 enzymes, DNMT3B3 and DNMT34 drive distinct types of chromatin compaction and patterns of histone 3 lysine 9 tri-methylation (H3K9me3) deposition. Our findings suggest that regulation of active DNMT3 members through the formation of co-complexes with inactive DNMT3 variants is a general mechanism by which DNMT3 variants function. This may account for some of the changes in DNA methylation patterns observed during development and disease.
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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.