ArticleProtein & cell2023
METTL14 is a chromatin regulator independent of its RNA N6-methyladenosine methyltransferase activity.
Article in Protein & cell, 2023. 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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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.
The trial behind it
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Who cites it
47 citing papers in PubMed, 76 citations in OpenAlex.
- mExperimental and therapeutic medicine · 2026Review
- mNature metabolism · 2026Article
- METTL14 Downregulation Accelerates HBV-Related Cirrhosis and Hepatocellular Carcinoma by Promoting Type I Interferon Release via the cGAS-STING Pathway Through mJournal of medical virology · 2026Article
- Spatially resolved mNature methods · 2026Article
- Advances in m6A Modification in Pregnancy-Related Disorders and Female Reproductive Endocrine Diseases.Expert reviews in molecular medicine · 2026Review
- METTL14 inhibits atherogenesis by epigenetically activating PPAR-α/γ transcription and fatty acid oxidation in VSMCs.Cardiovascular research · 2026Article
- Loss of METTL14 in dopaminergic neurons disrupts ER homeostasis via m6A-dependent regulation of Atp2a3 mRNA: Implications for Parkinson's Disease.NPJ Parkinson's disease · 2026Article
- Integrated epigenetic networks in aging: from histone to RNA modifications.Journal of translational medicine · 2026Review
- The Regulatory Role of mCells · 2026Review
- RM2Target v2.0: an updated database for the target genes of writers, erasers, and readers of RNA modifications.Nucleic acids research · 2026Article
- Epitranscriptomic control of epithelial-mesenchymal transition in cancer: mechanisms, plasticity, and therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- PSMC5 Orchestrates an Immunosuppressive Niche and Metastasis in Colorectal Cancer via SMURF1-Mediated K11-Linked Ubiquitination of METTL14.International journal of biological sciences · 2026Article
- Astrocytic Mettl14 depletion enhances cognitive function by attenuating astrogliosis via the DUSP1/MAPK pathway in APP/PS1 mice: targeting neuroinflammation in Alzheimer's disease.Molecular psychiatry · 2026Article
- The dual regulatory role of METTL14-mediated mFrontiers in oncology · 2026Review
- Marked for Success: How RNA mCellular and molecular gastroenterology and hepatology · 2026Review
- RNA modifications in cancer: from biological insights to therapeutic targets.Bioorganic & medicinal chemistry · 2026Review
- Advances in research on RNA methylation and its role in the immune microenvironment of gastrointestinal tumors.Frontiers in cell and developmental biology · 2026Review
- Histone lysine demethylases in breast cancer: molecular mechanisms, biological functions, and therapeutic intervention.Molecular cancer · 2025Review
- Functional and clinical significance of the RNA mNPJ breast cancer · 2025Article
- METTL3 and METTL14 determine human neural fate specifications.Nucleic acids research · 2025Article
Corrections and comments
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Authors and funding
18 authors at 7 institutions in 2 countries.
Funding
Abstract
METTL3 and METTL14 are two components that form the core heterodimer of the main RNA m6A methyltransferase complex (MTC) that installs m6A. Surprisingly, depletion of METTL3 or METTL14 displayed distinct effects on stemness maintenance of mouse embryonic stem cell (mESC). While comparable global hypo-methylation in RNA m6A was observed in Mettl3 or Mettl14 knockout mESCs, respectively. Mettl14 knockout led to a globally decreased nascent RNA synthesis, whereas Mettl3 depletion resulted in transcription upregulation, suggesting that METTL14 might possess an m6A-independent role in gene regulation. We found that METTL14 colocalizes with the repressive H3K27me3 modification. Mechanistically, METTL14, but not METTL3, binds H3K27me3 and recruits KDM6B to induce H3K27me3 demethylation independent of METTL3. Depletion of METTL14 thus led to a global increase in H3K27me3 level along with a global gene suppression. The effects of METTL14 on regulation of H3K27me3 is essential for the transition from self-renewal to differentiation of mESCs. This work reveals a regulatory mechanism on heterochromatin by METTL14 in a manner distinct from METTL3 and independently of m6A, and critically impacts transcriptional regulation, stemness maintenance, and differentiation of mESCs.
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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.