ArticleRNA (New York, N.Y.)2017
The cancer-associated U2AF35 470A>G (Q157R) mutation creates an in-frame alternative 5' splice site that impacts splicing regulation in Q157R patients.
Article in RNA (New York, N.Y.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- U2af1Leukemia · 2026Article
- Unveiling splicing disruptions due to common somatic variants in acute myeloid leukemia.Human genomics · 2025Article
- Rare occurrence of cryptic 5' splice sites by downstream 3' splice site/exon boundary mutations in a heavy-ion-inducedFrontiers in plant science · 2024Article
- Early Splicing Complexes and Human Disease.International journal of molecular sciences · 2023Review
- Recruitment of a splicing factor to the nuclear lamina for its inactivation.Communications biology · 2022Article
- Review
- Article
- The zinc finger domains in U2AF26 and U2AF35 have diverse functionalities including a role in controlling translation.RNA biology · 2020Article
- Differential Interleukin-2 Transcription Kinetics Render Mouse but Not Human T Cells Vulnerable to Splicing Inhibition Early after Activation.Molecular and cellular biology · 2019Article
- Increased versatility despite reduced molecular complexity: evolution, structure and function of metazoan splicing factor PRPF39.Nucleic acids research · 2019Article
- The cryo-EM structure of the SF3b spliceosome complex bound to a splicing modulator reveals a pre-mRNA substrate competitive mechanism of action.Genes & development · 2018Article
- Characterization of cis-acting elements that control oscillating alternative splicing.RNA biology · 2018Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent work has identified cancer-associated U2AF35 missense mutations in two zinc-finger (ZnF) domains, but little is known about Q157R/P substitutions within the second ZnF. Surprisingly, we find that the c.470A>G mutation not only leads to the Q157R substitution, but also creates an alternative 5' splice site (ss) resulting in the deletion of four amino acids (Q157Rdel). Q157P, Q157R, and Q157Rdel control alternative splicing of distinct groups of exons in cell culture and in human patients, suggesting that missplicing of different targets may contribute to cellular aberrations. Our data emphasize the importance to explore missense mutations beyond altered protein sequence.
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