ArticleThe Journal of experimental medicine2021
The mRNA m6A reader YTHDF2 suppresses proinflammatory pathways and sustains hematopoietic stem cell function.
Article in The Journal of experimental medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
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Who cites it
86 citing papers in PubMed, 142 citations in OpenAlex.
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- Methyltransferase-Like 14 Promotes the Angiogenesis of Hepatocellular Carcinoma via Targeting Vascular Endothelial Growth Factor A.Cancer reports (Hoboken, N.J.) · 2026Article
- Emerging role of RNA modification reader YTHDF2 in hematopoiesis, immunity, and cancer.MedScience · 2026Review
- NNature reviews. Cancer · 2026Review
- Downregulation of FTO aggravates osteoarthritis with obesity by erasing mMilitary Medical Research · 2026Article
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- HNRNPC-Mediated m6A Epitranscriptomics Drives CD80-Dependent Tubular Dysfunction in Sepsis-Induced AKI.Inflammation · 2025Article
- mCells · 2025Review
- METTL13 is essential for the survival of acute myeloid leukemia cells by regulating MYC.Cell death discovery · 2025Article
- METTL3 Promotes OSCC Progression by Down-Regulating WEE1 in a m6A-YTHDF2-Dependent Manner.Molecular biotechnology · 2025Article
- N6-Methyladenosine Modification in the Metabolic Dysfunction-Associated Steatotic Liver Disease.Nutrients · 2025Review
- RNA Modification and Digestive Tract Tumors: A Review.Current medicinal chemistry · 2025Review
- Single-cell transcriptome profiling of mMolecular biomedicine · 2024Article
- NMolecular medicine (Cambridge, Mass.) · 2024Review
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- Role of RNA modifications in blood development and regeneration.Experimental hematology · 2024Review
- Dynamic RNA methylation modifications and their regulatory role in mammalian development and diseases.Science China. Life sciences · 2024Review
- Reading the mCell & bioscience · 2024Review
26 more citing papers are in PubMed but not listed here.
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Authors and funding
19 authors at 6 institutions in 3 countries.
Funding
Abstract
The mRNA N6-methyladenosine (m6A) modification has emerged as an essential regulator of normal and malignant hematopoiesis. Inactivation of the m6A mRNA reader YTHDF2, which recognizes m6A-modified transcripts to promote m6A-mRNA degradation, results in hematopoietic stem cell (HSC) expansion and compromises acute myeloid leukemia. Here we investigate the long-term impact of YTHDF2 deletion on HSC maintenance and multilineage hematopoiesis. We demonstrate that Ythdf2-deficient HSCs from young mice fail upon serial transplantation, display increased abundance of multiple m6A-modified inflammation-related transcripts, and chronically activate proinflammatory pathways. Consistent with the detrimental consequences of chronic activation of inflammatory pathways in HSCs, hematopoiesis-specific Ythdf2 deficiency results in a progressive myeloid bias, loss of lymphoid potential, HSC expansion, and failure of aged Ythdf2-deficient HSCs to reconstitute multilineage hematopoiesis. Experimentally induced inflammation increases YTHDF2 expression, and YTHDF2 is required to protect HSCs from this insult. Thus, our study positions YTHDF2 as a repressor of inflammatory pathways in HSCs and highlights the significance of m6A in long-term HSC maintenance.
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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.