ArticlePLoS biology2020
Ribosome biogenesis is a downstream effector of the oncogenic U2AF1-S34F mutation.
Article in PLoS biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 21 citations in OpenAlex.
- PANoptosis in the pathogenesis of myelodysplastic syndromes.Molecular oncology · 2026Review
- Exploitation of host U2AF1 and U2AF2 splicing factors facilitates mosquito-borne orthoflavivirus infection across species.Nucleic acids research · 2026Article
- Article
- U2AF regulates the translation and localization of nuclear-encoded mitochondrial mRNAs.Molecular cell · 2026Article
- Phosphorylation-dependent regulation of serine/arginine-rich proteins and U2AF1 interactions in early spliceosome assembly.The Journal of biological chemistry · 2026Article
- Implications for metabolic disturbances in myelodysplastic syndromes.Seminars in hematology · 2024Review
- Aberrant pre-mRNA processing in cancer.The Journal of experimental medicine · 2024Review
- The selective prolyl hydroxylase inhibitor IOX5 stabilizes HIF-1α and compromises development and progression of acute myeloid leukemia.Nature cancer · 2024Article
- Upregulated expression ofJournal of gastrointestinal oncology · 2024Article
- Inhibition of epigenetic and cell cycle-related targets in glioblastoma cell lines reveals that onametostat reduces proliferation and viability in both normoxic and hypoxic conditions.Scientific reports · 2024Article
- U2AF1 in various neoplastic diseases and relevant targeted therapies for malignant cancers with complex mutations (Review).Oncology reports · 2024Review
- Full-length transcript alterations in human bronchial epithelial cells withLife science alliance · 2023Article
- Review
- The Biological and Clinical Consequences of RNA Splicing Factor U2AF1 Mutation in Myeloid Malignancies.Cancers · 2022Review
- Pre-mRNA splicing factor U2AF2 recognizes distinct conformations of nucleotide variants at the center of the pre-mRNA splice site signal.Nucleic acids research · 2022Article
- Identification of the hub genes related to adipose tissue metabolism of bovine.Frontiers in veterinary science · 2022Article
- Article
- SDE2 is an essential gene required for ribosome biogenesis and the regulation of alternative splicing.Nucleic acids research · 2021Article
- RNA-binding proteins of COSMIC importance in cancer.The Journal of clinical investigation · 2021Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
U2 Small Nuclear RNA Auxiliary Factor 1 (U2AF1) forms a heterodimeric complex with U2AF2 that is primarily responsible for 3' splice site selection. U2AF1 mutations have been identified in most cancers but are prevalent in Myelodysplastic Syndrome (MDS) and Acute Myeloid Leukemia (AML), and the most common mutation is a missense substitution of serine-34 to phenylalanine (S34F). The U2AF heterodimer also has a noncanonical function as a translational regulator. Here, we report that the U2AF1-S34F mutation results in specific misregulation of the translation initiation and ribosome biogenesis machinery. The net result is an increase in mRNA translation at the single-cell level. Among the translationally up-regulated targets of U2AF1-S34F is Nucleophosmin 1 (NPM1), which is a major driver of myeloid malignancy. Depletion of NPM1 impairs the viability of the U2AF1-S34F mutant cells and causes ribosomal RNA (rRNA) processing defects, thus indicating an unanticipated synthetic interaction between U2AF1, NPM1, and ribosome biogenesis. Our results establish a unique molecular phenotype for the U2AF1 mutation that recapitulates translational misregulation in myeloid disease.
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Registered trials
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.