ArticlePloS one2014
Schlafen 1 inhibits the proliferation and tube formation of endothelial progenitor cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The trial behind it
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
14 citing papers in PubMed.
- SLFN14 mutations underlie thrombocytopenia with excessive bleeding and platelet secretion defects.The Journal of clinical investigation · 2015Trial
- Schlafen 5 is an intracellular immune checkpoint and controls IFN responses in pancreatic ductal adenocarcinoma.JCI insight · 2026Article
- DIP2B as a Prognostic Biomarker and Immunotherapy Target: Insights from Pan-Cancer Analysis.Applied biochemistry and biotechnology · 2026Article
- Early hyperlipidemia triggers metabolomic reprogramming with increased SAH, increased acetyl-CoA-cholesterol synthesis, and decreased glycolysis.Redox biology · 2023Article
- Crowdsourcing temporal transcriptomic coronavirus host infection data: Resources, guide, and novel insights.Biology methods & protocols · 2023Article
- Schlafens Can Put Viruses to Sleep.Viruses · 2022Review
- Structural and biochemical characterization of human Schlafen 5.Nucleic acids research · 2022Article
- Robust Acquisition of Spatial Transcriptional Programs in Tissues With Immunofluorescence-Guided Laser Capture Microdissection.Frontiers in cell and developmental biology · 2022Article
- Review
- Global transcriptome study of Dip2B-deficient mouse embryonic lung fibroblast reveals its important roles in cell proliferation and development.Computational and structural biotechnology journal · 2020Article
- Splenic hematopoietic stem cells display a pre-activated phenotype.Immunology and cell biology · 2018Article
- Inhalation of Fine Particulate Matter Impairs Endothelial Progenitor Cell Function Via Pulmonary Oxidative Stress.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Schlafen 4-expressing myeloid-derived suppressor cells are induced during murine gastric metaplasia.The Journal of clinical investigation · 2016Article
- A Quantitative Proteomic Analysis of Hemogenic Endothelium Reveals Differential Regulation of Hematopoiesis by SOX17.Stem cell reports · 2015Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelial progenitor cells (EPCs) are the major source of cells that restore the endothelium during reendothelialization. This study was designed to investigate whether Schlafen 1 (Slfn1) has an effect on the proliferation and tube formation of EPCs in vivo. Slfn1 was expressed in rat EPCs. The overexpression of Slfn1 suppressed the proliferation and tube formation of EPCs; conversely, the knockdown of Slfn1 by shRNA promoted the proliferation and tube formation of EPCs. Furthermore, when Slfn1 was overexpressed, the EPCs were arrested in the G1 phase of the cell cycle. In contrast, when Slfn1 was knocked down, the EPCs progressed into the S phase of the cell cycle. Additionally, the overexpression of Slfn1 decreased the expression of Cyclin D1, whereas the knockdown of Slfn1 increased the expression of Cyclin D1; these findings suggest that Cyclin D1 is downstream of Slfn1 in Slfn1-mediated EPC proliferation. Taken together, these results indicate a key role for Slfn1 in the regulation of EPC biological behavior, which may provide a new target for the use of EPCs during reendothelialization.
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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.