ArticleCell death and differentiation2026
The m6A methyltransferase METTL14 promotes oncogenic Kras induced juvenile myelomonocytic leukemia through dysregulating autophagy.
Article in Cell death and differentiation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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Who cites it
3 citing papers in PubMed.
- Demethylase FTO attenuates atherosclerotic plaque via upregulating ABCA1 and ABCG1 expression by targeting ATG5.Molecular medicine reports · 2026Article
- The dual regulatory role of METTL14-mediated mFrontiers in oncology · 2026Review
- The role of RAS mutations in leukemia progression, differentiation, and drug resistance.Leukemia research reports · 2026Review
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Authors and funding
22 authors.
Funding
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Abstract
The N6-methyladenosine (m6A) modification plays an important role in the pathogenesis of various myeloid malignancies. However, its specific role in RAS mutation-induced myeloid malignancy is incompletely understood. In this study, we found that m6A methyltransferase methyltransferase-like 14 (METTL14) was highly expressed and associated with a shorter survival in a RAS-mutation myeloid malignancy, juvenile myelomonocytic leukemia (JMML). The knockout of METTL14 was revealed to significantly promote hematopoietic stem/progenitor cells (HSPCs) expansion and suppresses disease progression in a Kras
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