ArticlePLoS genetics2016
Wild-Type U2AF1 Antagonizes the Splicing Program Characteristic of U2AF1-Mutant Tumors and Is Required for Cell Survival.
Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed, 95 citations in OpenAlex.
- REAL-TIME VISUALIZATION OF SPLICEOSOME ASSEMBLY REVEALS BASIC PRINCIPLES OF 3' SPLICE SITE SELECTION.Research square · 2026Article
- U2AF1 mutations rescue deleterious exon skipping induced by KRAS mutations.Nature genetics · 2026Article
- Mutations in splicing factor gene U2AF1 rescue defective oncogene splicing in KRAS-mutant cancers.Nature genetics · 2026Article
- Role of alternative splicing in cancer progression.Irish journal of medical science · 2026Review
- 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
- Colorectal cancer-associated PCBP1 mutations disrupt protein stability in a dominant negative manner.bioRxiv : the preprint server for biology · 2025Article
- U2AF1 mutations rescue deleterious exon skipping induced by KRAS mutations.bioRxiv : the preprint server for biology · 2025Article
- Revealing the role of U2AF1 in splicing regulation and chimeric RNA dynamics.Scientific reports · 2025Article
- Splicing regulatory dynamics for precision analysis and treatment of heterogeneous leukemias.Science translational medicine · 2025Article
- From benign to pathogenic variants and vice versa: pyrimidine transitions at position -3 of TAG and CAG 3' splice sites.Journal of human genetics · 2025Article
- Recurrent Neurodevelopmentally Associated Variants of the Pre-mRNA Splicing Factor U2AF2 Alter RNA Binding Affinities and Interactions.Biochemistry · 2024Article
- The Role of CENPK Splice Variant in Abiraterone Response in Metastatic Castration-Resistant Prostate Cancer.Cells · 2024Article
- Article
- Comprehensive Analyses of the Effects of the Small-Molecule Inhibitor of the UHM Domain in the Splicing FactorResearch square · 2024Article
- R-Loop Accumulation in Spliceosome Mutant Leukemias Confers Sensitivity to PARP1 Inhibition by Triggering Transcription-Replication Conflicts.Cancer research · 2024Article
- Exonic splicing code and coordination of divalent metals in proteins.Nucleic acids research · 2024Article
- U2AF1 in various neoplastic diseases and relevant targeted therapies for malignant cancers with complex mutations (Review).Oncology reports · 2024Review
- Article
- Full-length transcript alterations in human bronchial epithelial cells withLife science alliance · 2023Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
We have asked how the common S34F mutation in the splicing factor U2AF1 regulates alternative splicing in lung cancer, and why wild-type U2AF1 is retained in cancers with this mutation. A human lung epithelial cell line was genetically modified so that U2AF1S34F is expressed from one of the two endogenous U2AF1 loci. By altering levels of mutant or wild-type U2AF1 in this cell line and by analyzing published data on human lung adenocarcinomas, we show that S34F-associated changes in alternative splicing are proportional to the ratio of S34F:wild-type gene products and not to absolute levels of either the mutant or wild-type factor. Preferential recognition of specific 3' splice sites in S34F-expressing cells is largely explained by differential in vitro RNA-binding affinities of mutant versus wild-type U2AF1 for those same 3' splice sites. Finally, we show that lung adenocarcinoma cell lines bearing U2AF1 mutations do not require the mutant protein for growth in vitro or in vivo. In contrast, wild-type U2AF1 is required for survival, regardless of whether cells carry the U2AF1S34F allele. Our results provide mechanistic explanations of the magnitude of splicing changes observed in U2AF1-mutant cells and why tumors harboring U2AF1 mutations always retain an expressed copy of the wild-type allele.
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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.