ArticleNature communications2019
Catalytically inactive Dnmt3b rescues mouse embryonic development by accessory and repressive functions.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
26 citing papers in PubMed, 49 citations in OpenAlex.
- Dnmt3b and Dnmt3l knockdown reduces blastocyst development in early mouse embryos.Histochemistry and cell biology · 2026Article
- Chromatin binding and N-terminal domains of DNMT3B1 confer specificity for developmentally regulated CpG island methylation.Genes & development · 2026Article
- Catalytic-independent roles of chromatin modifiers in mammalian development and the implications for treating human disease.Biochemical Society transactions · 2025Review
- Epigenetic mechanisms in maternal-fetal crosstalk: inter- and trans-generational inheritance.Epigenomics · 2025Review
- Molecular Regulation of Palatogenesis and Clefting: An Integrative Analysis of Genetic, Epigenetic Networks, and Environmental Interactions.International journal of molecular sciences · 2025Review
- A stepwise mode of TGFβ-SMAD signaling and DNA methylation regulates naïve-to-primed pluripotency and differentiation.Nature communications · 2024Article
- Using human disease mutations to understand de novo DNA methyltransferase function.Biochemical Society transactions · 2024Review
- DNA methylation restricts coordinated germline and neural fates in embryonic stem cell differentiation.Nature structural & molecular biology · 2024Article
- Epigenetic regulation of craniofacial development and disease.Birth defects research · 2024Review
- Tuning Methylation-Dependent Silencing Dynamics by Synthetic Modulation of CpG Density.ACS synthetic biology · 2023Article
- Tuning methylation-dependent silencing dynamics by synthetic modulation of CpG density.bioRxiv : the preprint server for biology · 2023Article
- Uterine deficiency of Dnmt3b impairs decidualization and causes consequent embryo implantation defects.Cell biology and toxicology · 2023Article
- DNMT3B supports meso-endoderm differentiation from mouse embryonic stem cells.Nature communications · 2023Article
- Mechanisms and function of de novo DNA methylation in placental development reveals an essential role for DNMT3B.Nature communications · 2023Article
- DNMT3B overexpression downregulates genes with CpG islands, common motifs, and transcription factor binding sites that interact with DNMT3B.Scientific reports · 2022Article
- Aberrant methylation of Serpine1 mediates lung injury in neonatal mice prenatally exposed to intrauterine inflammation.Cell & bioscience · 2022Article
- miR-539-5p regulatesMolecular therapy. Nucleic acids · 2022Article
- DNMT3A Harboring Leukemia-Associated Mutations Directs Sensitivity to DNA Damage at Replication Forks.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Tumor suppressor CEBPA interacts with and inhibits DNMT3A activity.Science advances · 2022Article
- Epigenetic Regulation in the Pathogenesis of Rheumatoid Arthritis.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
Abstract
DNA methylation regulates gene expression in a variety of processes, including mouse embryonic development. Four catalytically active enzymes function in mice as DNA methyltransferases (Dnmts) and as transcriptional regulators. Inactivation of Dnmt3b results in mouse embryonic lethality, but which activities are involved is unclear. Here we show that catalytically inactive Dnmt3b restores a majority of methylation and expression changes deregulated in the absence of Dnmt3b, and as a result, mice survive embryonic development. Thus, Dnmt3b functions as an accessory cofactor supporting catalytic activities performed by other Dnmts. We further demonstrate that Dnmt3b is linked to a control of major developmental pathways, including Wnt and hedgehog signaling. Dnmt3b directly represses Wnt9b whose aberrant up-regulation contributes to embryonic lethality of Dnmt3b knockout embryos. Our results highlight that Dnmt3b is a multifaceted protein that serves as an enzyme, an accessory factor for other methyltransferases, and as a transcriptional repressor in mouse embryogenesis.
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Registered trials
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.