ArticleBlood2011
Fine-tuning nucleophosmin in macrophage differentiation and activation.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 45 citations in OpenAlex.
- InstaNovo-P: a de novo peptide sequencing model for phosphoproteomics.Nature communications · 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
- Improving immunotherapy responses by dual inhibition of macrophage migration inhibitory factor and PD-1.JCI insight · 2025Article
- Combined bacterial translocation and cholestasis aggravates liver injury by activation pyroptosis in obstructive jaundice.Heliyon · 2024Article
- Establishment of a high-content compatible platform to assess effects of monocyte-derived factors on neural stem cell proliferation and differentiation.Scientific reports · 2024Article
- Caspase Inhibition Modulates Monocyte-Derived Macrophage Polarization in Damaged Tissues.International journal of molecular sciences · 2023Article
- The generation, activation, and polarization of monocyte-derived macrophages in human malignancies.Frontiers in immunology · 2023Review
- The kidney protects against sepsis by producing systemic uromodulin.American journal of physiology. Renal physiology · 2022Article
- Reprogramming monocyte-derived macrophages through caspase inhibition.Oncoimmunology · 2022Article
- Too much death can kill you: inhibiting intrinsic apoptosis to treat disease.The EMBO journal · 2021Review
- The role of caspase-8 in the tumor microenvironment of ovarian cancer.Cancer metastasis reviews · 2021Review
- Cathepsin B Is Required for NLRP3 Inflammasome Activation in Macrophages, Through NLRP3 Interaction.Frontiers in cell and developmental biology · 2020Article
- Leukemogenic nucleophosmin mutation disrupts the transcription factor hub that regulates granulomonocytic fates.The Journal of clinical investigation · 2018Article
- IL-34 and CSF-1 display an equivalent macrophage differentiation ability but a different polarization potential.Scientific reports · 2018Article
- The Role of Ubiquitination and Hepatocyte Growth Factor-Regulated Tyrosine Kinase Substrate in the Degradation of the Adrenomedullin Type I Receptor.Scientific reports · 2017Article
- Non-apoptotic functions of caspases in myeloid cell differentiation.Cell death and differentiation · 2017Review
- First-Breath-Induced Type 2 Pathways Shape the Lung Immune Environment.Cell reports · 2017Article
- Caspase-8 inhibition represses initial human monocyte activation in septic shock model.Oncotarget · 2016Article
- The PRKAA1/AMPKα1 pathway triggers autophagy during CSF1-induced human monocyte differentiation and is a potential target in CMML.Autophagy · 2015Article
- Dual regulation of SPI1/PU.1 transcription factor by heat shock factor 1 (HSF1) during macrophage differentiation of monocytes.Leukemia · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
M-CSF-driven differentiation of peripheral blood monocytes is one of the sources of tissue macrophages. In humans and mice, the differentiation process involves the activation of caspases that cleave a limited number of proteins. One of these proteins is nucleophosmin (NPM1), a multifunctional and ubiquitous protein. Here, we show that caspases activated in monocytes exposed to M-CSF cleave NPM1 at D213 to generate a 30-kDa N-terminal fragment. The protein is further cleaved into a 20-kDa fragment, which involves cathepsin B. NPM1 fragments contribute to the limited motility, migration, and phagocytosis capabilities of resting macrophages. Their activation with lipopolysaccharides inhibits proteolytic processes and restores expression of the full-length protein that negatively regulates the transcription of genes encoding inflammatory cytokines (eg, NPM1 is recruited with NF-κB on the MCP1 gene promoter to decrease its transcription). In mice with heterozygous npm gene deletion, cytokine production in response to lipopolysaccharides, including CXCL1 (KC), MCP1, and MIP2, is dramatically enhanced. These results indicate a dual function of NPM1 in M-CSF-differentiated macrophages. Proteolysis of the protein participates in the establishment of a mature macrophage phenotype. In response to inflammatory stimuli, the full-length protein negatively regulates inflammatory cytokine production.
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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.