ArticleEpigenetics & chromatin2021
Ethionine-mediated reduction of S-adenosylmethionine is responsible for the neural tube defects in the developing mouse embryo-mediated m6A modification and is involved in neural tube defects via modulating Wnt/β-catenin signaling pathway.
Article in Epigenetics & chromatin, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Epigenetic Perspectives on Maternal Gut Microbiota's Impact on Embryonic and Fetal Development.Comprehensive Physiology · 2026Review
- NNature reviews. Cancer · 2026Review
- The role of chrysanthemum phytochemicals in neural tube development: a narrative review of underlying mechanisms.Frontiers in cell and developmental biology · 2026Review
- N6-methyladenosine methylation: a novel key to unlocking mental disorders.The international journal of neuropsychopharmacology · 2025Review
- Mechanisms and rationales of SAM homeostasis.Trends in biochemical sciences · 2025Review
- Application of methylation in the diagnosis of ankylosing spondylitis.Clinical rheumatology · 2024Review
- FOXD3-mediated transactivation of ALKBH5 promotes neuropathic pain via mProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Advances in brain epitranscriptomics research and translational opportunities.Molecular psychiatry · 2024Review
- Melatonin alleviates valproic acid-induced neural tube defects by modulating Src/PI3K/ERK signaling and oxidative stress.Acta biochimica et biophysica Sinica · 2024Article
- Expression profiling of N6-methyladenosine-modified mRNA in PC12 cells in response to unconjugated bilirubin.Molecular biology reports · 2023Article
- The Regulatory Network of METTL3 in the Nervous System: Diagnostic Biomarkers and Therapeutic Targets.Biomolecules · 2023Review
- Abnormal methylation caused by folic acid deficiency in neural tube defects.Open life sciences · 2022Review
- Identifying key mFrontiers in genetics · 2022Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neural tube defects (NTDs) remain one of the most life-threatening birth defects affecting infants. Most patients with NTDs eventually develop lifelong disability, which cause significant morbidity and mortality and seriously reduce the quality of life. Our previous study has found that ethionine inhibits cell viability by disrupting the balance between proliferation and apoptosis, and preventing neural stem cells from differentiating into neurons and astrocytes. However, how ethionine participates in the pathogenesis of neural tube development through N6-methyladenosine (m6A) modification remains unknown. This study aims to investigate METTL3- and ALKBH5-mediated m6A modification function and mechanism in NTDs. Herein, our results demonstrate that SAM play not only a compensatory role, it also leads to changes of m6A modification in neural tube development and regulation. Additionally, these data implicate that METTL3 is enriched in HT-22 cells, and METTL3 knockdown reduces cell proliferation and increases apoptosis through suppressing Wnt/β-catenin signaling pathway. Significantly, overexpression of ALKBH5 can only inhibit cell proliferation, but cannot promote cell apoptosis. This research reveals an important role of SAM in development of NTDs, providing a good theoretical basis for further research on NTDs. This finding represents a novel epigenetic mechanism underlying that the m6A modification has profound and lasting implications for neural tube development.
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