ArticlePloS one2011
Macrophage activation and differentiation signals regulate schlafen-4 gene expression: evidence for Schlafen-4 as a modulator of myelopoiesis.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 103 citations in OpenAlex.
- SLFN14 mutations underlie thrombocytopenia with excessive bleeding and platelet secretion defects.The Journal of clinical investigation · 2015Trial
- Integrated proteogenomic profiling reveals coordinated differential expression signatures during neuroinflammation.Acta neuropathologica communications · 2026Article
- RadiotherapyTranslational lung cancer research · 2025Article
- SLFN14 functions as a P-TEFb inhibitor to modulate the transcription of HIV-1 and cellular genes.Science advances · 2025Article
- SLFN11, far from being limited to responding to cancer DNA damage.Clinical and experimental medicine · 2025Review
- Experimental Murine Periodontitis Increases Salivary Gland IgA-Producing B Cells Following Oral Dysbiosis.Microbiology and immunology · 2025Article
- Exploring the Therapeutic Potential of Extracellular Vesicles Anchored to the Sea Cucumber Extracellular Matrix for Treating Atopic Dermatitis.Biomaterials research · 2025Article
- Transcriptional analysis of cancer cachexia: conserved and unique features across preclinical models and biological sex.American journal of physiology. Cell physiology · 2024Article
- Momordicine-I Suppresses Head and Neck Cancer Growth by Reprogrammimg Immunosuppressive Effect of the Tumor-Infiltrating Macrophages and B Lymphocytes.Molecular cancer therapeutics · 2024Article
- Overview of Structural and Functional Insights of SLFN12 Associated With Different Diseases.Cureus · 2024Review
- Myocardial Matrix Hydrogels Mitigate Negative Remodeling and Improve Function in Right Heart Failure Model.JACC. Basic to translational science · 2024Article
- Research progress of the SLFN family in malignant tumors.Frontiers in oncology · 2024Review
- Transcriptomic analysis reveals that RasGEF1b deletion alters basal and LPS-induced expression of genes involved in chemotaxis and cytokine responses in macrophages.Scientific reports · 2023Article
- Schlafen-5 inhibits LINE-1 retrotransposition.iScience · 2023Article
- Differences in gene regulation by TLR3 and IPS-1 signaling in murine corneal epithelial cells.Scientific reports · 2023Article
- HDAC7 is an immunometabolic switch triaging danger signals for engagement of antimicrobial versus inflammatory responses in macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Novel Prediction Method Applied to Wound Age Estimation: Developing a Stacking Ensemble Model to Improve Predictive Performance Based on Multi-mRNA.Diagnostics (Basel, Switzerland) · 2023Article
- Schlafen4Frontiers in immunology · 2023Article
- Toll-like Receptor 9 Pathway Mediates SchlafenGastroenterology · 2022Article
- Structural, molecular, and functional insights into Schlafen proteins.Experimental & molecular medicine · 2022Review
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe ten mouse and six human members of the Schlafen (Slfn) gene family all contain an AAA domain. Little is known of their function, but previous studies suggest roles in immune cell development. In this report, we assessed Slfn regulation and function in macrophages, which are key cellular regulators of innate immunity. METHODOLOGY/PRINCIPAL
findingsMultiple members of the Slfn family were up-regulated in mouse bone marrow-derived macrophages (BMM) by the Toll-like Receptor (TLR)4 agonist lipopolysaccharide (LPS), the TLR3 agonist Poly(I∶C), and in disease-affected joints in the collagen-induced model of rheumatoid arthritis. Of these, the most inducible was Slfn4. TLR agonists that signal exclusively through the MyD88 adaptor protein had more modest effects on Slfn4 mRNA levels, thus implicating MyD88-independent signalling and autocrine interferon (IFN)-β in inducible expression. This was supported by the substantial reduction in basal and LPS-induced Slfn4 mRNA expression in IFNAR-1⁻/⁻ BMM. LPS causes growth arrest in macrophages, and other Slfn family genes have been implicated in growth control. Slfn4 mRNA levels were repressed during macrophage colony-stimulating factor (CSF-1)-mediated differentiation of bone marrow progenitors into BMM. To determine the role of Slfn4 in vivo, we over-expressed the gene specifically in macrophages in mice using a csf1r promoter-driven binary expression system. Transgenic over-expression of Slfn4 in myeloid cells did not alter macrophage colony formation or proliferation in vitro. Monocyte numbers, as well as inflammatory macrophages recruited to the peritoneal cavity, were reduced in transgenic mice that specifically over-expressed Slfn4, while macrophage numbers and hematopoietic activity were increased in the livers and spleens.
conclusionsSlfn4 mRNA levels were up-regulated during macrophage activation but down-regulated during differentiation. Constitutive Slfn4 expression in the myeloid lineage in vivo perturbs myelopoiesis. We hypothesise that the down-regulation of Slfn4 gene expression during macrophage differentiation is a necessary step in development of this lineage.
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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.