ArticleNature medicine2010
A p53-dependent mechanism underlies macrocytic anemia in a mouse model of human 5q- syndrome.
Article in Nature medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 177 papers, 1 of them a synthesis that pooled it.
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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
177 citing papers in PubMed, 1 synthesis or guideline pooled it, 331 citations in OpenAlex.
- The Coming of Age of Preclinical Models of MDS.Frontiers in oncology · 2022Pooled it
- Trial
- Pan-cancer multi-omics analysis reveals upregulation of the POLE2 subunit of DNA polymerase epsilon and its associations with patient survival and cellular pathways beyond DNA replication.NAR genomics and bioinformatics · 2026Article
- Mutant ribosomal protein RPS15 drives B cell malignancy through oxidative stress and genomic instability.Nature communications · 2026Article
- Biomarkers and advances in AML-MRC: from bench to bedside.Annals of hematology · 2026Review
- Clinical and Biological Insights into Myelodysplastic Neoplasms Associated with Deletions of Chromosome 5q Region.Hematology reports · 2025Review
- Article
- Interacting Fat1 and Dchs Planar Cell Polarity Proteins Supported by Fjx1 Serve as Heterodimeric Intercellular Bridges Crucial to Support Spermatogenesis.Advances in experimental medicine and biology · 2025Review
- Analyzing the role of ferroptosis in ribosome-related bone marrow failure disorders: From pathophysiology to potential pharmacological exploitation.IUBMB life · 2024Review
- An atypical form of 60S ribosomal subunit in Diamond-Blackfan anemia linked to RPL17 variants.JCI insight · 2024Article
- Single-cell transcriptional profile of CD34+ hematopoietic progenitor cells from del(5q) myelodysplastic syndromes and impact of lenalidomide.Nature communications · 2024Article
- Mcph1, mutated in primary microcephaly, is also crucial for erythropoiesis.EMBO reports · 2024Article
- ABIN1 (Q478) is Required to Prevent Hematopoietic Deficiencies through Regulating Type I IFNs Expression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Review
- Animal models of Diamond-Blackfan anemia: updates and challenges.Haematologica · 2023Review
- Review
- Understanding the Continuum between High-Risk Myelodysplastic Syndrome and Acute Myeloid Leukemia.International journal of molecular sciences · 2023Review
- Ribosome biogenesis and function in development and disease.Development (Cambridge, England) · 2023Review
- Serotonergic neuron ribosomal proteins regulate the neuroendocrine control of Drosophila development.PLoS genetics · 2022Article
- Decoding the pathogenesis of Diamond-Blackfan anemia using single-cell RNA-seq.Cell discovery · 2022Article
117 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
The identification of the genes associated with chromosomal translocation breakpoints has fundamentally changed understanding of the molecular basis of hematological malignancies. By contrast, the study of chromosomal deletions has been hampered by the large number of genes deleted and the complexity of their analysis. We report the generation of a mouse model for human 5q- syndrome using large-scale chromosomal engineering. Haploinsufficiency of the Cd74-Nid67 interval (containing Rps14, encoding the ribosomal protein S14) caused macrocytic anemia, prominent erythroid dysplasia and monolobulated megakaryocytes in the bone marrow. These effects were associated with defective bone marrow progenitor development, the appearance of bone marrow cells expressing high amounts of the tumor suppressor p53 and increased bone marrow cell apoptosis. Notably, intercrossing with p53-deficient mice completely rescued the progenitor cell defect, restoring common myeloid progenitor and megakaryocytic-erythroid progenitor, granulocyte-monocyte progenitor and hematopoietic stem cell bone marrow populations. This mouse model suggests that a p53-dependent mechanism underlies the pathophysiology of the 5q- syndrome.
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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.