ArticlePloS one2013
Transcriptome analysis of the zebrafish model of Diamond-Blackfan anemia from RPS19 deficiency via p53-dependent and -independent pathways.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 25 citations in OpenAlex.
- Red lines and green lights: Gene therapy for inherited erythroid disorders beyond the haemoglobinopathies.British journal of haematology · 2026Review
- DNA Methylation Episignature as a Novel Diagnostic Tool for Diamond-Blackfan Anemia Syndrome.American journal of hematology · 2026Article
- Article
- Ribosomal biogenesis defects trigger subunit specific developmental checkpoints via TOR signaling and gap junction in C. elegans.Developmental biology · 2026Article
- Review
- Nucleolar Protein 56 Deficiency in Zebrafish Leads to Developmental Abnormalities and Anemia viaBiology · 2023Article
- Article
- Targeting elevated heme levels to treat a mouse model for Diamond-Blackfan Anemia.Experimental hematology · 2022Article
- Rcl1 depletion impairs 18S pre-rRNA processing at the A1-site and up-regulates a cohort of ribosome biogenesis genes in zebrafish.Nucleic acids research · 2021Article
- Loss ofG3 (Bethesda, Md.) · 2019Article
- Modeling hematopoietic disorders in zebrafish.Disease models & mechanisms · 2019Review
- Innate immune system activation in zebrafish and cellular models of Diamond Blackfan Anemia.Scientific reports · 2018Article
- Article
- Modeling Myeloid Malignancies Using Zebrafish.Frontiers in oncology · 2017Review
- Transcriptome analysis reveals a ribosome constituents disorder involved in the RPL5 downregulated zebrafish model of Diamond-Blackfan anemia.BMC medical genomics · 2016Article
- The Ribosome Biogenesis Protein Nol9 Is Essential for Definitive Hematopoiesis and Pancreas Morphogenesis in Zebrafish.PLoS genetics · 2015Article
- 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
- Ribosomal Protein Mutations Result in Constitutive p53 Protein Degradation through Impairment of the AKT Pathway.PLoS genetics · 2015Article
- Systematic transcriptome analysis of the zebrafish model of diamond-blackfan anemia induced by RPS24 deficiency.BMC genomics · 2014Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diamond-Blackfan anemia (DBA) is a rare inherited bone marrow failure syndrome that is characterized by pure red-cell aplasia and associated physical deformities. It has been proven that defects of ribosomal proteins can lead to this disease and that RPS19 is the most frequently mutated gene in DBA patients. Previous studies suggest that p53-dependent genes and pathways play important roles in RPS19-deficient embryos. However, whether there are other vital factors linked to DBA has not been fully clarified. In this study, we compared the whole genome RNA-Seq data of zebrafish embryos injected with RPS19 morpholino (RPS19 MO), RPS19 and p53 morpholino simultaneously (RPS19+p53 MO) and control morpholino (control). We found that genes enriched in the functions of hematological systems, nervous system development and skeletal and muscular disorders had significant differential expression in RPS19 MO embryos compared with controls. Co-inhibition of p53 partially alleviates the abnormalities for RPS19-deficient embryos. However, the hematopoietic genes, which were down-regulated significantly in RPS19 MO embryos, were not completely recovered by the co-inhibition of p53. Furthermore, we identified the genome-wide p53-dependent and -independent genes and pathways. These results indicate that not only p53 family members but also other factors have important impacts on RPS19-deficient embryos. The detection of potential pathogenic genes and pathways provides us a new paradigm for future research on DBA, which is a systematic and complex hereditary disease.
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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.