ArticleNature communications2019
Adult stem cell deficits drive Slc29a3 disorders in mice.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
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
27 citing papers in PubMed, 49 citations in OpenAlex.
- Functional SLC29A3/ENT3 drives autophagic clearance of intracellular viral particles.Virus research · 2026Article
- Article
- The lysosomal carrier SLC29A3 supports antibacterial signaling, and promotes autophagy by activating TRPML1 in murine dendritic cells.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Allogeneic hematopoietic cell transplantation rescues congenital red cell aplasia in H syndrome due toHaematologica · 2025Article
- The lysosomal catabolism of nucleic acids-critical regulators of the innate immune system.Nucleic acids research · 2025Review
- Direction and modality of transcription changes caused by TAD boundary disruption in Slc29a3/Unc5b locus depends on tissue-specific epigenetic context.Epigenetics & chromatin · 2025Article
- Review
- Clinical Progression and Manifestations of H Syndrome: A Case Report of Failed Treatment Option.The American journal of case reports · 2024Article
- Targeting Solute Carrier Transporters (SLCs) as a Therapeutic Target in Different Cancers.Diseases (Basel, Switzerland) · 2024Review
- Rheumatological complaints in H syndrome: from inflammatory profiling to target treatment in a case study.Pediatric rheumatology online journal · 2024Article
- H syndrome mimicking Erdheim Chester disease: new entity and therapeutic perspectives.Haematologica · 2023Article
- MBROLE3: improved functional enrichment of chemical compounds for metabolomics data analysis.Nucleic acids research · 2023Article
- Increased renal elimination of endogenous and synthetic pyrimidine nucleosides in concentrative nucleoside transporter 1 deficient mice.Nature communications · 2023Article
- IFN-stimulated metabolite transporter ENT3 facilitates viral genome release.EMBO reports · 2023Article
- Nucleoside transporters and immunosuppressive adenosine signaling in the tumor microenvironment: Potential therapeutic opportunities.Pharmacology & therapeutics · 2022Review
- Inborn Errors of Nucleoside Transporter (NT)-Encoding Genes (International journal of molecular sciences · 2022Review
- Solute Carrier Nucleoside Transporters in Hematopoiesis and Hematological Drug Toxicities: A Perspective.Cancers · 2022Review
- Red cell adenylate kinase deficiency in China: molecular study of 2 new mutations (413G > A, 223dupA).BMC medical genomics · 2022Article
- Regulation of the nucleic acid-sensing Toll-like receptors.Nature reviews. Immunology · 2022Review
- Article
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 4 institutions in 1 country.
Funding
Abstract
Mutations exclusively in equilibrative nucleoside transporter 3 (ENT3), the only intracellular nucleoside transporter within the solute carrier 29 (SLC29) gene family, cause an expanding spectrum of human genetic disorders (e.g., H syndrome, PHID syndrome, and SHML/RDD syndrome). Here, we identify adult stem cell deficits that drive ENT3-related abnormalities in mice. ENT3 deficiency alters hematopoietic and mesenchymal stem cell fates; the former leads to stem cell exhaustion, and the latter leads to breaches of mesodermal tissue integrity. The molecular pathogenesis stems from the loss of lysosomal adenosine transport, which impedes autophagy-regulated stem cell differentiation programs via misregulation of the AMPK-mTOR-ULK axis. Furthermore, mass spectrometry-based metabolomics and bioenergetics studies identify defects in fatty acid utilization, and alterations in mitochondrial bioenergetics can additionally propel stem cell deficits. Genetic, pharmacologic and stem cell interventions ameliorate ENT3-disease pathologies and extend the lifespan of ENT3-deficient mice. These findings delineate a primary pathogenic basis for the development of ENT3 spectrum disorders and offer critical mechanistic insights into treating human ENT3-related disorders.
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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.