ArticleNature communications2017
DEK-targeting DNA aptamers as therapeutics for inflammatory arthritis.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 2 of them syntheses that pooled it.
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.
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
66 citing papers in PubMed, 2 syntheses or guidelines pooled it, 102 citations in OpenAlex.
- Delving into the clinical impact of NETs in pediatric cancer.Pediatric research · 2025Pooled it
- Application of aptamers in regenerative medicine.Frontiers in bioengineering and biotechnology · 2022Pooled it
- DEK Loss Induces Task-specific Deficits in Learning and Memory and Reprograms the Hippocampal Transcriptome in Mice.Molecular neurobiology · 2026Article
- Neutrophils and neutrophil extracellular traps in diabetes mellitus and its complications: Mechanisms and therapeutic implications.iScience · 2026Review
- Aptamers Targeting IL17A and Its Receptor Suppress IL17 Signaling in Different Cell Types.Pharmaceuticals (Basel, Switzerland) · 2026Article
- A comprehensive insight into NETosis-extracellular vesicle crosstalk in autoimmune diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Neutrophil Extracellular Traps (NETs) in health and disease.Molecular biomedicine · 2025Review
- Advanced Nanoparticle Therapeutics for Targeting Neutrophils in Inflammatory Diseases.Advanced healthcare materials · 2025Review
- Deficiency of DEK proto-oncogene alleviates allergic rhinitis by inhibiting RhoA/Ezrin-mediated mitochondrial fission.Animal models and experimental medicine · 2025Article
- DNA-Based Hydrogels for Musculoskeletal Reconstruction: Harnessing Dynamic Programmability and Multimodal Therapeutic Integration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- NUP214 in Acute Myeloid Leukemia.Cells · 2025Review
- Exploring the involvement of serine proteases in neutrophil extracellular traps: a review of mechanisms and implications.Cell death & disease · 2025Review
- Antibody and aptamer-based therapies for osteoarthritis: Application of antibodies and promise of aptamers.Molecular therapy. Nucleic acids · 2025Review
- Proto-oncogene DEK binds to pre-mRNAs and regulates the alternative splicing of Hippo signaling genes in HeLa cells.Molecular genetics and genomics : MGG · 2025Article
- Inhibition of DEK restores hematopoietic stem cell function in Fanconi anemia.The Journal of experimental medicine · 2025Article
- The emerging role of neutrophil extracellular traps in autoimmune and autoinflammatory diseases.MedComm · 2025Review
- New Insights into Potential Therapeutic Targets for Neuroendocrine Prostate Cancer: From Bench to Clinic.Research (Washington, D.C.) · 2025Review
- Review
- Therapeutic Exploitation of Neuroendocrine Transdifferentiation Drivers in Prostate Cancer.Cells · 2024Review
- Neutrophil extracellular traps in homeostasis and disease.Signal transduction and targeted therapy · 2024Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
20 authors at 2 institutions in 1 country.
Funding
Abstract
Novel therapeutics are required for improving the management of chronic inflammatory diseases. Aptamers are single-stranded RNA or DNA molecules that have recently shown utility in a clinical setting, as they can specifically neutralize biomedically relevant proteins, particularly cell surface and extracellular proteins. The nuclear chromatin protein DEK is a secreted chemoattractant that is abundant in the synovia of patients with juvenile idiopathic arthritis (JIA). Here, we show that DEK is crucial to the development of arthritis in mouse models, thus making it an appropriate target for aptamer-based therapy. Genetic depletion of DEK or treatment with DEK-targeted aptamers significantly reduces joint inflammation in vivo and greatly impairs the ability of neutrophils to form neutrophil extracellular traps (NETs). DEK is detected in spontaneously forming NETs from JIA patient synovial neutrophils, and DEK-targeted aptamers reduce NET formation. DEK is thus key to joint inflammation, and anti-DEK aptamers hold promise for the treatment of JIA and other types of arthritis.
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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 Socratic graph.