ArticleCellular and molecular life sciences : CMLS2020
Tet3 regulates cellular identity and DNA methylation in neural progenitor cells.
Article in Cellular and molecular life sciences : CMLS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 31 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
31 citing papers in PubMed, 42 citations in OpenAlex.
- Molecular interactome of HNRNPU reveals regulatory networks in neuronal differentiation and DNA methylation.Nucleic acids research · 2026Article
- Genome-wide demethylation and targeted remethylation during metamorphosis in the jewel wasp Nasonia vitripennis.Epigenetics & chromatin · 2025Article
- OAC1 improves mitofusin 2 expression to alleviate neuronal injury following experimental ischemic stroke.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Article
- Roles of PEG10 in cancer and neurodegenerative disorder (Review).Oncology reports · 2025Review
- Zuogui Pills Improve the Learning and Memory Ability of Brain-Aging Mice through the Estrogen Receptor ERα Methylation Pathway.Combinatorial chemistry & high throughput screening · 2025Article
- Potential therapeutic targets for ischemic stroke in pre-clinical studies: Epigenetic-modifying enzymes DNMT/TET and HAT/HDAC.Frontiers in pharmacology · 2025Review
- Interactions of Polychlorinated Biphenyls and Their Metabolites with the Brain and Liver Transcriptome of Female Mice.ACS chemical neuroscience · 2024Article
- Recent Advances and Therapeutic Implications of 2-Oxoglutarate-Dependent Dioxygenases in Ischemic Stroke.Molecular neurobiology · 2024Review
- Catalytic-dependent and -independent roles of TET3 in the regulation of specific genetic programs during neuroectoderm specification.Communications biology · 2024Article
- Inhibition of myocardial remodeling through miR-150/TET3 axis after AMI.Molecular biology reports · 2023Article
- Aberrant Expression of TET2 Accounts for DNA Hypomethylation in Varicocele.Cell journal · 2023Article
- TET1-TRPV4 Signaling Contributes to Bone Cancer Pain in Rats.Brain sciences · 2023Article
- Review
- Deficiency of Tet3 in nucleus accumbens enhances fear generalization and anxiety-like behaviors in mice.Brain pathology (Zurich, Switzerland) · 2022Article
- Targeted erasure of DNA methylation by TET3 drives adipogenic reprogramming and differentiation.Nature metabolism · 2022Article
- New Insights into TETs in Psychiatric Disorders.International journal of molecular sciences · 2022Review
- Two families with TET3-related disorder showing neurodevelopmental delay with craniofacial dysmorphisms.Journal of human genetics · 2022Article
- The Epigenetic Role of Vitamin C in Neurodevelopment.International journal of molecular sciences · 2022Review
- Differential Expression of Steroid Hormone Receptors and Ten Eleven Translocation Proteins in Endometrial Cancer Cells.Frontiers in oncology · 2022Article
- Structure and Function of TET Enzymes.Advances in experimental medicine and biology · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
Abstract
TET enzymes oxidize 5-methylcytosine (5mC) into 5-hydroxymethylcytosine (5hmC), a process thought to be intermediary in an active DNA demethylation mechanism. Notably, 5hmC is highly abundant in the brain and in neuronal cells. Here, we interrogated the function of Tet3 in neural precursor cells (NPCs), using a stable and inducible knockdown system and an in vitro neural differentiation protocol. We show that Tet3 is upregulated during neural differentiation, whereas Tet1 is downregulated. Surprisingly, Tet3 knockdown led to a de-repression of pluripotency-associated genes such as Oct4, Nanog or Tcl1, with concomitant hypomethylation. Moreover, in Tet3 knockdown NPCs, we observed the appearance of OCT4-positive cells forming cellular aggregates, suggesting de-differentiation of the cells. Notably, Tet3 KD led to a genome-scale loss of DNA methylation and hypermethylation of a smaller number of CpGs that are located at neurogenesis-related genes and at imprinting control regions (ICRs) of Peg10, Zrsr1 and Mcts2 imprinted genes. Overall, our results suggest that TET3 is necessary to maintain silencing of pluripotency genes and consequently neural stem cell identity, possibly through regulation of DNA methylation levels in neural precursor cells.
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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.