ArticleBlood2005
An RNA interference model of RPS19 deficiency in Diamond-Blackfan anemia recapitulates defective hematopoiesis and rescue by dexamethasone: identification of dexamethasone-responsive genes by microarray.
Article in Blood, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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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
41 citing papers in PubMed, 91 citations in OpenAlex.
- NOC4L coordinates neuronal and pharyngeal arch development by regulating ribosome biogenesis.Journal of molecular cell biology · 2026Article
- Temporal Regulation of Cytokines and Growth Factors for Optimized Hematopoietic-Lineage Specification from Human Pluripotent Stem Cells.International journal of stem cells · 2025Article
- Article
- Hacking hematopoiesis - emerging tools for examining variant effects.Disease models & mechanisms · 2023Article
- An RPS19-edited model for Diamond-Blackfan anemia reveals TP53-dependent impairment of hematopoietic stem cell activity.JCI insight · 2023Article
- Erythroid lineage-specific lentiviral RNAi vectors suitable for molecular functional studies and therapeutic applications.Scientific reports · 2022Article
- Stem Cells in the Myelodysplastic Syndromes.Frontiers in aging · 2021Review
- Identification of novel drug targets for diamond-blackfan anemia based on RPS19 gene mutation using protein-protein interaction network.BMC systems biology · 2018Article
- Revealing nascent proteomics in signaling pathways and cell differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Protein arginine methyltransferase 6 controls erythroid gene expression and differentiation of human CD34Haematologica · 2018Article
- RPL27A is a target of miR-595 and may contribute to the myelodysplastic phenotype through ribosomal dysgenesis.Oncotarget · 2016Article
- Glucocorticoids improve erythroid progenitor maintenance and dampen Trp53 response in a mouse model of Diamond-Blackfan anaemia.British journal of haematology · 2015Article
- Ribosomopathies: how a common root can cause a tree of pathologies.Disease models & mechanisms · 2015Review
- PPAR-α and glucocorticoid receptor synergize to promote erythroid progenitor self-renewal.Nature · 2015Article
- Marrow failure: a window into ribosome biology.Blood · 2014Review
- Role of Rho kinases in abnormal and normal hematopoiesis.Current opinion in hematology · 2014Review
- Ribosomopathies: mechanisms of disease.Clinical medicine insights. Blood disorders · 2014Review
- Clinical and hematologic manifestations in patients with Diamond Blackfan anemia in Korea.The Korean journal of hematology · 2012Article
- Stress granules contribute to α-globin homeostasis in differentiating erythroid cells.Biochemical and biophysical research communications · 2012Article
- canSAR: an integrated cancer public translational research and drug discovery resource.Nucleic acids research · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Diamond-Blackfan anemia (DBA), a congenital erythroblastopenia, is a model disease for the study of erythroid differentiation but is poorly understood. RPS19 is the only gene yet to have been associated with DBA, but its relevance to erythroid differentiation is unclear. The molecular basis for the stimulation of erythropoiesis by glucocorticoids in patients with DBA has not been identified. We demonstrate that targeted degradation of the RPS19 transcript, through retroviral expression of short hairpin RNAs (shRNAs), blocks the proliferation and differentiation of erythroid progenitor cells in cultured human CD34(+) cells. Treatment of RPS19-deficient cells with dexamethasone restores erythroid differentiation to normal levels. We investigated the molecular basis of pharmacologic therapies for DBA using oligonucleotide microarrays to survey gene expression in CD34(+) cells treated with combinations of dexamethasone, erythropoietin, stem cell factor, and interleukin-3. Dexamethasone did not alter expression of RPS19 but activated a genetic program that includes a set of key hematopoietic regulatory genes. Genes specific to erythroid progenitor cells were up-regulated by dexamethasone, while genes specific to nonerythroid lineages were down-regulated. Deficiency of RPS19 therefore blocks proliferation of immature erythroid progenitor cells, and dexamethasone activates proliferation of the same cell population through mechanisms independent of RPS19.
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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.