ArticleBiochimica et biophysica acta2009
Ribosomal protein S19 and S24 insufficiency cause distinct cell cycle defects in Diamond-Blackfan anemia.
Article in Biochimica et biophysica acta, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 48 citations in OpenAlex.
- Stabilized marker gene identification and functional annotation from single-cell transcriptomic data.PLoS computational biology · 2025Article
- Decoding the pathogenesis of Diamond-Blackfan anemia using single-cell RNA-seq.Cell discovery · 2022Article
- Review
- Article
- A uniparental isodisomy event introducing homozygous pathogenic variants drives a multisystem metabolic disorder.Cold Spring Harbor molecular case studies · 2019Article
- Article
- Identification of genes and pathways in the synovia of women with osteoarthritis by bioinformatics analysis.Molecular medicine reports · 2018Article
- Translating the Game: Ribosomes as Active Players.Frontiers in genetics · 2018Review
- Ribosomal protein NtRPL17 interacts with kinesin-12 family protein NtKRP and functions in the regulation of embryo/seed size and radicle growth.Journal of experimental botany · 2017Article
- Osteosarcoma: Molecular Pathogenesis and iPSC Modeling.Trends in molecular medicine · 2017Review
- Up-regulation of small nucleolar RNA 78 is correlated with aggressive phenotype and poor prognosis of hepatocellular carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Structure of human MDM2 complexed with RPL11 reveals the molecular basis of p53 activation.Genes & development · 2015Article
- PRPF8 defects cause missplicing in myeloid malignancies.Leukemia · 2015Article
- Regulatory role of small nucleolar RNAs in human diseases.BioMed research international · 2015Review
- Systematic transcriptome analysis of the zebrafish model of diamond-blackfan anemia induced by RPS24 deficiency.BMC genomics · 2014Article
- Article
- Primary hematopoietic cells from DBA patients with mutations in RPL11 and RPS19 genes exhibit distinct erythroid phenotype in vitro.Cell death & disease · 2012Article
- Transcriptomic analysis of the clam Meretrix meretrix on different larval stages.Marine biotechnology (New York, N.Y.) · 2012Article
- Ddx18 is essential for cell-cycle progression in zebrafish hematopoietic cells and is mutated in human AML.Blood · 2011Article
- Untangling the phenotypic heterogeneity of Diamond Blackfan anemia.Seminars in hematology · 2011Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Diamond-Blackfan anemia (DBA) is a severe congenital anemia characterized by a specific decrease of erythroid precursors. The disease is also associated with growth retardation, congenital malformations, a predisposition for malignant disease and heterozygous mutations in either of the ribosomal protein (RP) genes RPS7, RPS17, RPS19, RPS24, RPL5, RPL11 and RPL35a. We show herein that primary fibroblasts from DBA patients with truncating mutations in RPS19 or in RPS24 have a marked reduction in proliferative capacity. Mutant fibroblasts are associated with extended cell cycles and normal levels of p53 when compared to w.t. cells. RPS19 mutant fibroblasts accumulate in the G1 phase, whereas the RPS24 mutant cells show an altered progression in the S phase resulting in reduced levels in the G2/M phase. RPS19 deficient cells exhibit reduced levels of Cyclin-E, CDK2 and retinoblastoma (Rb) protein supporting a cell cycle arrest in the G1 phase. In contrast, RPS24 deficient cells show increased levels of the cell cycle inhibitor p21 and a seemingly opposing increase in Cyclin-E, CDK4 and CDK6. In combination, our results show that RPS19 and RPS24 insufficient fibroblasts have an impaired growth caused by distinct blockages in the cell cycle. We suggest this proliferative constraint to be an important contributing mechanism for the complex extra-hematological features observed in DBA.
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