ArticleThe Journal of experimental medicine2012
A novel murine model of myeloproliferative disorders generated by overexpression of the transcription factor NF-E2.
Article in The Journal of experimental medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 2 of them syntheses that pooled it.
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Who cites it
51 citing papers in PubMed, 2 syntheses or guidelines pooled it, 72 citations in OpenAlex.
- Comparison and Implications of Mutational Profiles of Myelodysplastic Syndromes, Myeloproliferative Neoplasms, and Myelodysplastic/Myeloproliferative Neoplasms: A Meta-Analysis.Frontiers in oncology · 2020Pooled it
- Pooled it
- A novel role for transcription factor NFE2 in redox regulation and chemotherapy resistance in acute myeloid leukemia.Leukemia · 2026Article
- NFE2 Truncation Mutants Protect Wild-Type NFE2 from ITCH-Dependent Degradation.International journal of molecular sciences · 2025Article
- `Inflammatory mediators differentially regulate megakaryopoiesis and thrombopoiesis in myelofibrosis and essential thrombocythemia.Scientific reports · 2025Article
- [Clinical and molecular characteristics of myeloproliferative neoplasms patients with NFE2 gene mutations].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2025Article
- Lysine-specific demethylase 1 regulates hematopoietic stem cell expansion and myeloid cell differentiation.Cell death & disease · 2025Article
- CoREST in pieces: Dismantling the CoREST complex for cancer therapy and beyond.Science advances · 2025Review
- Clonal evolution of the 3D chromatin landscape in patients with relapsed pediatric B-cell acute lymphoblastic leukemia.Nature communications · 2024Article
- The histone demethylase JMJD2C constitutes a novel NFE2 target gene that is required for the survival of JAK2Leukemia · 2023Article
- Epigenetics in myeloproliferative neoplasms.Frontiers in oncology · 2023Review
- A Proliferation-Inducing Ligand and B-Cell Activating Factor Are Upregulated in Patients with Essential Thrombocythemia.Journal of clinical medicine · 2022Article
- Genetic Background of Polycythemia Vera.Genes · 2022Review
- The Cross Marks the Spot: The Emerging Role of JmjC Domain-Containing Proteins in Myeloid Malignancies.Biomolecules · 2021Review
- Concomitant constitutive LNK and NFE2 mutation with loss of sumoylation in a case of hereditary thrombocythemia.Haematologica · 2021Article
- PRMT5 Inhibition Modulates E2F1 Methylation and Gene-Regulatory Networks Leading to Therapeutic Efficacy in JAK2Cancer discovery · 2020Article
- Involvement of a Transcription factor,Cancers · 2020Article
- Givinostat: an emerging treatment for polycythemia vera.Expert opinion on investigational drugs · 2020Review
- Enhanced expression of the sphingosine-1-phosphate-receptor-3 causes acute myelogenous leukemia in mice.Leukemia · 2020Article
- Jmjd1c is dispensable for healthy adult hematopoiesis and Jak2V617F-driven myeloproliferative disease initiation in mice.PloS one · 2020Article
Corrections and comments
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Authors and funding
23 authors at 7 institutions in 4 countries.
Funding
Abstract
The molecular pathophysiology of myeloproliferative neoplasms (MPNs) remains poorly understood. Based on the observation that the transcription factor NF-E2 is often overexpressed in MPN patients, independent of the presence of other molecular aberrations, we generated mice expressing an NF-E2 transgene in hematopoietic cells. These mice exhibit many features of MPNs, including thrombocytosis, leukocytosis, Epo-independent colony formation, characteristic bone marrow histology, expansion of stem and progenitor compartments, and spontaneous transformation to acute myeloid leukemia. The MPN phenotype is transplantable to secondary recipient mice. NF-E2 can alter histone modifications, and NF-E2 transgenic mice show hypoacetylation of histone H3. Treatment of mice with the histone deacetylase inhibitor (HDAC-I) vorinostat restored physiological levels of histone H3 acetylation, decreased NF-E2 expression, and normalized platelet numbers. Similarly, MPN patients treated with an HDAC-I exhibited a decrease in NF-E2 expression. These data establish a role for NF-E2 in the pathophysiology of MPNs and provide a molecular rationale for investigating epigenetic alterations as novel targets for rationally designed MPN therapies.
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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.