ArticleBlood2019
Chromatin occupancy and epigenetic analysis reveal new insights into the function of the GATA1 N terminus in erythropoiesis.
Article in Blood, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 49 citations in OpenAlex.
- A quantitative dissection of the DNA-binding properties of pathogenic GATA1 mutants.The FEBS journal · 2026Article
- Quantitative analysis of DNA-GATA1 binding alterations linked to hematopoietic disorders.The FEBS journal · 2026Article
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- ZEB1 drives terminal erythroid maturation by controlling the GATA2-KLF1 regulatory switch.Nucleic acids research · 2026Article
- Article
- Advances in the characterization of in vitro-generated red blood cells: from biophysical properties to functional applications.Stem cell research & therapy · 2025Review
- Splicing of erythroid transcription factor is associated with therapeutic response in myelodysplastic syndromes.The Journal of clinical investigation · 2025Article
- Brd4 expression in CD4 T cells and in microglia promotes neuroinflammation in experimental autoimmune encephalomyelitis.Journal of neuroinflammation · 2025Article
- Baf155 controls hematopoietic differentiation and regeneration through chromatin priming.Cell reports · 2024Article
- Down syndrome and leukemia: from basic mechanisms to clinical advances.Haematologica · 2023Review
- Gata1s mutant mice display persistent defects in the erythroid lineage.Blood advances · 2023Article
- Layered immunity and layered leukemogenicity: Developmentally restricted mechanisms of pediatric leukemia initiation.Immunological reviews · 2023Review
- RUNX1 isoform disequilibrium promotes the development of trisomy 21-associated myeloid leukemia.Blood · 2023Article
- Leukemogenesis in infants and young children with trisomy 21.Hematology. American Society of Hematology. Education Program · 2022Article
- Mechanism of KIT gene regulation by GATA1 lacking the N-terminal domain in Down syndrome-related myeloid disorders.Scientific reports · 2022Article
- Stepwise GATA1 and SMC3 mutations alter megakaryocyte differentiation in a Down syndrome leukemia model.The Journal of clinical investigation · 2022Article
- Enhancers regulate 3' end processing activity to control expression of alternative 3'UTR isoforms.Nature communications · 2022Article
- Targeting GATA1 and p2x7r Locus Binding in Spinal Astrocytes Suppresses Chronic Visceral Pain by Promoting DNA Demethylation.Neuroscience bulletin · 2022Article
- Article
- Epigenetic and Transcriptional Control of Erythropoiesis.Frontiers in genetics · 2022Review
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17 authors at 4 institutions in 3 countries.
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Abstract
Mutations in GATA1, which lead to expression of the GATA1s isoform that lacks the GATA1 N terminus, are seen in patients with Diamond-Blackfan anemia (DBA). In our efforts to better understand the connection between GATA1s and DBA, we comprehensively studied erythropoiesis in Gata1s mice. Defects in yolks sac and fetal liver hematopoiesis included impaired terminal maturation and reduced numbers of erythroid progenitors. RNA-sequencing revealed that both erythroid and megakaryocytic gene expression patterns were altered by the loss of the N terminus, including aberrant upregulation of Gata2 and Runx1. Dysregulation of global H3K27 methylation was found in the erythroid progenitors upon loss of N terminus of GATA1. Chromatin-binding assays revealed that, despite similar occupancy of GATA1 and GATA1s, there was a striking reduction of H3K27me3 at regulatory elements of the Gata2 and Runx1 genes. Consistent with the observation that overexpression of GATA2 has been reported to impair erythropoiesis, we found that haploinsufficiency of Gata2 rescued the erythroid defects of Gata1s fetuses. Together, our integrated genomic analysis of transcriptomic and epigenetic signatures reveals that, Gata1 mice provide novel insights into the role of the N terminus of GATA1 in transcriptional regulation and red blood cell maturation which may potentially be useful for DBA patients.
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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.