ArticleBlood2010
AML1 is overexpressed in patients with myeloproliferative neoplasms and mediates JAK2V617F-independent overexpression of NF-E2.
Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 52 citations in OpenAlex.
- 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
- A Coordinated Translational Control Mediated by eEF2 Phosphorylation Safeguards Erythroid Differentiation.International journal of molecular sciences · 2025Article
- Genomic landscape of patients with germline RUNX1 variants and familial platelet disorder with myeloid malignancy.Blood advances · 2024Article
- Immune checkpoints represent a promising breakthrough in targeted therapy and prognosis of myelodysplastic syndrome.Heliyon · 2023Review
- Epigenetics in myeloproliferative neoplasms.Frontiers in oncology · 2023Review
- Genetic Background of Polycythemia Vera.Genes · 2022Review
- CIGB-300-Regulated Proteome Reveals Common and Tailored Response Patterns of AML Cells to CK2 Inhibition.Frontiers in molecular biosciences · 2022Article
- The Cross Marks the Spot: The Emerging Role of JmjC Domain-Containing Proteins in Myeloid Malignancies.Biomolecules · 2021Review
- Megakaryopoiesis and Platelet Biology: Roles of Transcription Factors and Emerging Clinical Implications.International journal of molecular sciences · 2021Review
- The Role of Neutrophilic Granulocytes in Philadelphia Chromosome Negative Myeloproliferative Neoplasms.International journal of molecular sciences · 2021Review
- Hydroxycarbamide effects on DNA methylation and gene expression in myeloproliferative neoplasms.Genome research · 2021Article
- A Broad Overview of Signaling inCancers · 2021Review
- Recent insights regarding the molecular basis of myeloproliferative neoplasms.The Korean journal of internal medicine · 2020Review
- LSD1 Inhibition Prolongs Survival in Mouse Models of MPN by Selectively Targeting the Disease Clone.HemaSphere · 2018Article
- Article
- MYC-dependent recruitment of RUNX1 and GATA2 on the SET oncogene promoter enhances PP2A inactivation in acute myeloid leukemia.Oncotarget · 2017Article
- Nuclear Factor Erythroid 2 Regulates Human HSC Self-Renewal and T Cell Differentiation by Preventing NOTCH1 Activation.Stem cell reports · 2017Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
The transcription factor NF-E2 is overexpressed in the majority of patients with polycythemia vera (PV). Concomitantly, 95% of these patients carry the JAK2(V617F) mutation. Although NF-E2 levels correlate with JAK2(V671F) allele burden in some PV cohorts, the molecular mechanism causing aberrant NF-E2 expression has not been described. Here we show that NF-E2 expression is also increased in patients with essential thrombocythemia and primary myelofibrosis independent of the presence of the JAK2(V617F) mutation. Characterization of the NF-E2 promoter revealed multiple functional binding sites for AML1/RUNX-1. Chromatin immunoprecipitation demonstrated AML1 binding to the NF-E2 promoter in vivo. Moreover, AML1 binding to the NF-E2 promoter was significantly increased in granulocytes from PV patients compared with healthy controls. AML1 mRNA expression was elevated in patients with PV, essential thrombocythemia, and primary myelofibrosis both in the presence and absence of JAK2(V617F). In addition, AML1 and NF-E2 expression were highly correlated. RNAi-mediated suppression of either AML1 or of its binding partner CBF-beta significantly decreased NF-E2 expression. Moreover, expression of the leukemic fusion protein AML/ETO drastically decreased NF-E2 protein levels. Our data identify NF-E2 as a novel AML1 target gene and delineate a role for aberrant AML1 expression in mediating elevated NF-E2 expression in MPN patients.
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