ArticleJournal of cellular and molecular medicine2019
Knockdown of spliceosome U2AF1 significantly inhibits the development of human erythroid cells.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- The oncogene protein kinase PIM1 regulates mammalian erythroblast enucleation.Communications biology · 2025Article
- Mutational Spectrum and Clinical Outcomes of Myelodysplastic/Myeloproliferative Neoplasms: A Single-Institution Study in Korea with Emphasis onJournal of clinical medicine · 2025Article
- Revealing the role of U2AF1 in splicing regulation and chimeric RNA dynamics.Scientific reports · 2025Article
- Intramedullary erythrophagocytosis in myelodysplastic syndrome with heterozygous U2AF1 Q157R variant.EJHaem · 2025Article
- Post-transcriptional regulation of erythropoiesis.Blood science (Baltimore, Md.) · 2023Review
- U2AF1 and EZH2 mutations are associated with nonimmune hemolytic anemia in myelodysplastic syndromes.Blood advances · 2023Article
- U2af1 is a haplo-essential gene required for hematopoietic cancer cell survival in mice.The Journal of clinical investigation · 2021Article
- Differential U2AF1 mutation sites, burden and co-mutation genes can predict prognosis in patients with myelodysplastic syndrome.Scientific reports · 2020Article
- Knockdown of spliceosome U2AF1 significantly inhibits the development of human erythroid cells.Journal of cellular and molecular medicine · 2019Article
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
U2AF1 (U2AF35) is the small subunit of the U2 auxiliary factor (U2AF) that constitutes the U2 snRNP (small nuclear ribonucleoproteins) of the spliceosome. Here, we examined the function of U2AF1 in human erythropoiesis. First, we examined the expression of U2AF1 during in vitro human erythropoiesis and showed that U2AF1 was highly expressed in the erythroid progenitor burst-forming-unit erythroid (BFU-E) cell stage. A colony assay revealed that U2AF1 knockdown cells failed to form BFU-E and colony-forming-unit erythroid (CFU-E) colonies. Our results further showed that knockdown of U2AF1 significantly inhibited cell growth and induced apoptosis in erythropoiesis. Additionally, knockdown of U2AF1 also delayed terminal erythroid differentiation. To explore the molecular basis of the impaired function of erythroid development, RNA-seq was performed and the Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis results showed that several biological pathways, including the p53 signalling pathway, MAPK signalling pathway and haematopoietic cell lineage, were involved, with the p53 signalling pathway showing the greatest involvement. Western blot analysis revealed an increase in the protein levels of downstream targets of p53 following U2AF1 knockdown. The data further showed that depletion of U2AF1 altered alternatively spliced apoptosis-associated gene transcripts in CFU-E cells. Our findings elucidate the role of U2AF1 in human erythropoiesis and reveal the underlying mechanisms.
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