ArticleNature communications2020
ETNK1 mutations induce a mutator phenotype that can be reverted with phosphoethanolamine.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 48 citations in OpenAlex.
- Biosynthesis of Phosphatidylethanolamine and Phosphatidylcholine via the Kennedy Pathway in Cancer and Other Pathological Conditions.International journal of molecular sciences · 2026Review
- Targeting the microglial phosphatidylethanolamine synthesis pathway promotes GABARAP-associated phagocytosis and Aβ clearance in Alzheimer's disease.Signal transduction and targeted therapy · 2026Article
- Integrated proteomics and metabolomics reveal phytosesquiterpene lactones inhibit TNBC cell activity by depleting ATP synthesis and reprogramming primary metabolism.Scientific reports · 2026Article
- Phosphoethanolamine: a translational journey from biological process and physiopathological effects to therapeutical innovation - a mini-review.Frontiers in pharmacology · 2026Review
- Identification of circulating miRNA alterations in diabetes patients excluding periodontitis effects: insights into target gene downregulation in diabetic complications.Annals of medicine · 2025Article
- Atypical chronic myeloid leukemia: From diagnosis to molecular features and therapeutic options.HemaSphere · 2025Review
- The role of carnitine palmitoyl transferase 2 in the progression of salt-sensitive hypertension.American journal of physiology. Cell physiology · 2025Article
- Targeted LC-MS profiling reveals dysregulated glycolytic flux and TCA cycle stalling in POAG plasma.Scientific reports · 2025Article
- Integrative single-cell metabolomics and phenotypic profiling reveals metabolic heterogeneity of cellular oxidation and senescence.Nature communications · 2025Article
- EGCG and DOX dual-drug-loaded enzyme-responsive nanovesicles boost mitochondrial-mediated ICD for improved immunotherapy.Frontiers in pharmacology · 2025Article
- Epigenome-wide methylation analysis shows phosphonoethylamine alleviates aberrant DNA methylation in NASH caused by Pcyt2 deficiency.PloS one · 2025Article
- Can molecular patterns help to classify overlapping entities in myeloid neoplasms?Histopathology · 2025Review
- Molecular and clinical characterization of ETNK1-mutated myeloid neoplasms: the Mayo Clinic experience.Blood advances · 2024Article
- DNA methylation patterns in the frontal lobe white matter of multiple system atrophy, Parkinson's disease, and progressive supranuclear palsy: a cross-comparative investigation.Acta neuropathologica · 2024Article
- Applying Multiomics to Basosquamous Carcinoma.The Journal of investigative dermatology · 2024Article
- Article
- Mechanism of Action and Translational Potential of (Stroke · 2024Article
- A homoeostatic switch causing glycerol-3-phosphate and phosphoethanolamine accumulation triggers senescence by rewiring lipid metabolism.Nature metabolism · 2024Article
- Lipid profiling of RON and DEK-dependent signaling in breast cancer guides discovery of gene networks predictive of poor outcomes.Frontiers in oncology · 2024Article
- Case report: Safety and efficacy of synergistic treatment using selinexor and azacitidine in patients with atypical chronic myeloid leukemia with resistance to decitabine.Frontiers in oncology · 2024Article
Corrections and comments
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Authors and funding
30 authors at 7 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recurrent somatic mutations in ETNK1 (Ethanolamine-Kinase-1) were identified in several myeloid malignancies and are responsible for a reduced enzymatic activity. Here, we demonstrate in primary leukemic cells and in cell lines that mutated ETNK1 causes a significant increase in mitochondrial activity, ROS production, and Histone H2AX phosphorylation, ultimately driving the increased accumulation of new mutations. We also show that phosphoethanolamine, the metabolic product of ETNK1, negatively controls mitochondrial activity through a direct competition with succinate at mitochondrial complex II. Hence, reduced intracellular phosphoethanolamine causes mitochondria hyperactivation, ROS production, and DNA damage. Treatment with phosphoethanolamine is able to counteract complex II hyperactivation and to restore a normal phenotype.
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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.