ArticleScientific reports2016
H2AX deficiency is associated with erythroid dysplasia and compromised haematopoietic stem cell function.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Article
- The effect of U2AF1 mutation on erythroid differentiation and sensitivity to demethylation drug treatment.Medical oncology (Northwood, London, England) · 2025Article
- DNA damage signalling histone H2AX is required for tumour growth.Cell death discovery · 2024Article
- Iron chelation improves ineffective erythropoiesis and iron overload in myelodysplastic syndrome mice.eLife · 2023Article
- Kindlin-3 deficiency leads to impaired erythropoiesis and erythrocyte cytoskeleton.Blood advances · 2023Article
- Histone H2A.X phosphorylation and Caspase-Initiated Chromatin Condensation in late-stage erythropoiesis.Epigenetics & chromatin · 2021Article
- Oxidative DNA Damage, Inflammatory Signature, and Altered Erythrocytes Properties in Diamond-Blackfan Anemia.International journal of molecular sciences · 2020Article
- Loss of mDia1 causes neutropenia via attenuated CD11b endocytosis and increased neutrophil adhesion to the endothelium.Blood advances · 2017Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Myelodysplastic syndromes (MDS) are clonal disorders of haematopoiesis characterised by dysplastic changes of major myeloid cell lines. However, the mechanisms underlying these dysplastic changes are poorly understood. Here, we used a genetically modified mouse model and human patient data to examine the physiological roles of H2AX in haematopoiesis and how the loss of H2AX contributes to dyserythropoiesis in MDS. H2AX knockout mice showed cell-autonomous anaemia and erythroid dysplasia, mimicking dyserythropoiesis in MDS. Also, dyserythropoiesis was increased in MDS patients with the deletion of chromosome 11q23, where H2AX is located. Although loss of H2AX did not affect the early stage of terminal erythropoiesis, enucleation was decreased. H2AX deficiency also led to the loss of quiescence of hematopoietic stem and progenitor cells, which dramatically compromised their bone marrow engraftment. These results reveal important roles of H2AX in late-stage terminal erythropoiesis and hematopoietic stem cell function.
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Registered trials
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