ArticlePLoS genetics2019
NPM and NPM-MLF1 interact with chromatin remodeling complexes and influence their recruitment to specific genes.
Article in PLoS genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Article
- Identification of cryptic KMT2A-PTD and other novel fusion genes by transcriptome sequencing alters molecular risk stratification in AML-NK.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Nucleophosmin 1 proteins as potential therapeutic targets in non-communicable chronic inflammatory diseases: a review of pathophysiological mechanisms.Frontiers in cell and developmental biology · 2026Review
- Phase-separating fusion proteins drive cancer by upsetting transcription regulation.Genome biology · 2025Article
- Downregulation of MLF1 safeguards cardiomyocytes against senescence-associated chromatin opening.Nucleic acids research · 2025Article
- NPM3 as an Unfavorable Prognostic Biomarker Involved in Oncogenic Pathways of Lung AdenocarcinomaCombinatorial chemistry & high throughput screening · 2024Article
- An Updated Overview of the Role of CYP450 during Xenobiotic Metabolization in Regulating the Acute Myeloid Leukemia Microenvironment.International journal of molecular sciences · 2023Review
- Combinatorial genetics reveals the Dock1-Rac2 axis as a potential target for the treatment of NPM1;Cohesin mutated AML.Leukemia · 2022Article
- Functional characterization of NPM1-TYK2 fusion oncogene.NPJ precision oncology · 2022Article
- IKAROS is required for the measured response of NOTCH target genes upon external NOTCH signaling.PLoS genetics · 2021Article
- Clinical implications of recurrent gene mutations in acute myeloid leukemia.Experimental hematology & oncology · 2020Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Nucleophosmin (NPM1) is frequently mutated or subjected to chromosomal translocation in acute myeloid leukemia (AML). NPM protein is primarily located in the nucleus, but the recurrent NPMc+ mutation, which creates a nuclear export signal, is characterized by cytoplasmic localization and leukemogenic properties. Similarly, the NPM-MLF1 translocation product favors the partial cytoplasmic retention of NPM. Regardless of their common cellular distribution, NPM-MLF1 malignancies engender different effects on hematopoiesis compared to NPMc+ counterparts, highlighting possible aberrant nuclear function(s) of NPM in NPMc+ and NPM-MLF1 AML. We performed a proteomic analysis and found that NPM and NPM-MLF1 interact with various nuclear proteins including subunits of the chromatin remodeling complexes ISWI, NuRD and P/BAF. Accordingly, NPM and NPM-MLF1 are recruited to transcriptionally active or repressed genes along with NuRD subunits. Although the overall gene expression program in NPM knockdown cells is similar to that resulting from NPMc+, NPM-MLF1 expression differentially altered gene transcription regulated by NPM. The abnormal gene regulation imposed by NPM-MLF1 can be characterized by the enhanced recruitment of NuRD to gene regulatory regions. Thus, different mechanisms would orchestrate the dysregulation of NPM function in NPMc+- versus NPM1-MLF1-associated leukemia.
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Registered trials
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