ArticleLeukemia2019
Rps14, Csnk1a1 and miRNA145/miRNA146a deficiency cooperate in the clinical phenotype and activation of the innate immune system in the 5q- syndrome.
Article in Leukemia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 51 citations in OpenAlex.
- Aberrant Kupffer-like differentiation of hematopoietic stem cell is critical for the MDS pathogenesis in Setd2-deficient mice.Cell death and differentiation · 2026Article
- Critical role of niche S100A8 for acute myeloid leukemia progression and hematopoiesis regeneration.Blood advances · 2025Article
- Clinical and Biological Insights into Myelodysplastic Neoplasms Associated with Deletions of Chromosome 5q Region.Hematology reports · 2025Review
- An inflammatory T-cell-stromal axis contributes to hematopoietic stem/progenitor cell failure and clonal evolution in human myelodysplastic syndrome.Nature communications · 2025Article
- Review
- Bone marrow microenvironment in myelodysplastic neoplasms: insights into pathogenesis, biomarkers, and therapeutic targets.Cancer cell international · 2025Review
- Exploring Ribosomal Genes as Potential Biomarkers of the Immune Microenvironment in Respiratory Syncytial Virus Infection.Biochemical genetics · 2025Article
- Article
- High throughput transcriptomics analysis of ovine mammary epithelial cells stimulated with Staphylococcus aureus in vitro.PloS one · 2025Article
- Bone marrow inflammation in haematological malignancies.Nature reviews. Immunology · 2024Review
- Inactivation of p53 provides a competitive advantage to del(5q) myelodysplastic syndrome hematopoietic stem cells during inflammation.Haematologica · 2023Article
- Diagnosis of Myelodysplastic Syndromes: From Immunological Observations to Clinical Applications.Diagnostics (Basel, Switzerland) · 2022Review
- Pathophysiologic and clinical implications of molecular profiles resultant from deletion 5q.EBioMedicine · 2022Article
- Genetic barcoding systematically compares genes in del(5q) MDS and reveals a central role for CSNK1A1 in clonal expansion.Blood advances · 2022Article
- Downregulation of ZNF280A inhibits proliferation and tumorigenicity of colorectal cancer cells by promoting the ubiquitination and degradation of RPS14.Frontiers in oncology · 2022Article
- Eukaryotic ribosome quality control system: a potential therapeutic target for human diseases.International journal of biological sciences · 2022Review
- p53 Activation in Genetic Disorders: Different Routes to the Same Destination.International journal of molecular sciences · 2021Review
- Innate immune pathways and inflammation in hematopoietic aging, clonal hematopoiesis, and MDS.The Journal of experimental medicine · 2021Review
- Heterogeneous bone-marrow stromal progenitors drive myelofibrosis via a druggable alarmin axis.Cell stem cell · 2021Article
- Blockade of IL-22 signaling reverses erythroid dysfunction in stress-induced anemias.Nature immunology · 2021Article
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RPS14, CSNK1A1, and miR-145 are universally co-deleted in the 5q- syndrome, but mouse models of each gene deficiency recapitulate only a subset of the composite clinical features. We analyzed the combinatorial effect of haploinsufficiency for Rps14, Csnk1a1, and miRNA-145, using mice with genetically engineered, conditional heterozygous inactivation of Rps14 and Csnk1a1 and stable knockdown of miR-145/miR-146a. Combined Rps14/Csnk1a1/miR-145/146a deficiency recapitulated the cardinal features of the 5q- syndrome, including (1) more severe anemia with faster kinetics than Rps14 haploinsufficiency alone and (2) pathognomonic megakaryocyte morphology. Macrophages, regulatory cells of erythropoiesis and the innate immune response, were significantly increased in Rps14/Csnk1a1/miR-145/146a deficient mice as well as in 5q- syndrome patient bone marrows and showed activation of the innate immune response, reflected by increased expression of S100A8, and decreased phagocytic function. We demonstrate that Rps14/Csnk1a1/miR-145 and miR-146a deficient macrophages alter the microenvironment and induce S100A8 expression in the mesenchymal stem cell niche. The increased S100A8 expression in the mesenchymal niche was confirmed in 5q- syndrome patients. These data indicate that intrinsic defects of the 5q- syndrome hematopoietic stem cell directly alter the surrounding microenvironment, which in turn affects hematopoiesis as an extrinsic mechanism.
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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.