ReviewNucleic acids research2020
Hallmarks of ribosomopathies.
Review in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 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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Who cites it
139 citing papers in PubMed, 190 citations in OpenAlex.
- Illuminating ribosome biogenesis disorders through structural biology.RNA biology · 2026Review
- Article
- An Epstein-Barr virus-encoded snoRNA directs 2'-O-methylation of human rRNAs to control translation and the viral lytic switch.Cell reports · 2026Article
- The potential of gene therapy to rescue telomeric and extratelomeric defects in X-linked dyskeratosis congenita.Molecular therapy. Advances · 2026Article
- RPS27L Maintains Nucleolar Homeostasis to Regulate Proliferation and Differentiation of Bovine Skeletal Muscle Satellite Cells.Animals : an open access journal from MDPI · 2026Article
- A small nucleolar RNA dictates the structure and function of translating ribosomes in Leishmania.Nature communications · 2026Article
- RiboScreenBiomedicines · 2026Review
- NOC4L coordinates neuronal and pharyngeal arch development by regulating ribosome biogenesis.Journal of molecular cell biology · 2026Article
- Understanding and Overcoming Osteosarcoma Heterogeneity.Biomolecules · 2026Review
- Article
- Ribosomal protein eL22 contributes to the assembly of 60S ribosomal subunits inbioRxiv : the preprint server for biology · 2026Article
- A three generation family with VACTERL association is found to have a rare form of diamond-blackfan anaemia.European journal of human genetics : EJHG · 2026Article
- RPS19 and RPL5 haploinsufficient models reveal divergent ribosomal subunit controls of fetal hematopoiesis.Nature communications · 2026Article
- Hydroxyl radical footprinting modification reveals an intradomain communication pathway in EFL1 disrupted by a Shwachman-Diamond syndrome-associated mutation.Protein science : a publication of the Protein Society · 2026Article
- Mutant ribosomal protein RPS15 drives B cell malignancy through oxidative stress and genomic instability.Nature communications · 2026Article
- The EHMT2-MBLAC2 axis suppresses ribosomal DNA transcription in response to nucleolar DNA damage.Cell death & disease · 2026Article
- Distinct steps of nuclear maturation of human pre-60S complexes require the activity of GTPases including GNL3L.Nucleic acids research · 2026Article
- In silico mapping of non-canonical DNA structures across the human ribosomal DNA locus.G3 (Bethesda, Md.) · 2026Article
- Fibrillarin: bridging ribosome biogenesis and apoptosis in cellular stress and disease.Apoptosis : an international journal on programmed cell death · 2026Review
- Review
79 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ribosomopathies are diseases caused by defects in ribosomal constituents or in factors with a role in ribosome assembly. Intriguingly, congenital ribosomopathies display a paradoxical transition from early symptoms due to cellular hypo-proliferation to an elevated cancer risk later in life. Another association between ribosome defects and cancer came into view after the recent discovery of somatic mutations in ribosomal proteins and rDNA copy number changes in a variety of tumor types, giving rise to somatic ribosomopathies. Despite these clear connections between ribosome defects and cancer, the molecular mechanisms by which defects in this essential cellular machinery are oncogenic only start to emerge. In this review, the impact of ribosomal defects on the cellular function and their mechanisms of promoting oncogenesis are described. In particular, we discuss the emerging hallmarks of ribosomopathies such as the appearance of 'onco-ribosomes' that are specialized in translating oncoproteins, dysregulation of translation-independent extra-ribosomal functions of ribosomal proteins, rewired cellular protein and energy metabolism, and extensive oxidative stress leading to DNA damage. We end by integrating these findings in a model that can provide an explanation how ribosomopathies could lead to the transition from hypo- to hyper-proliferation in bone marrow failure syndromes with elevated cancer risk.
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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.