ArticleScientific reports2018
hnRNP A1/A2 and Sam68 collaborate with SRSF10 to control the alternative splicing response to oxaliplatin-mediated DNA damage.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 65 citations in OpenAlex.
- SRSF10 promotes cisplatin resistance in bladder cancer via BIN1 Exon 12 retention and ANXA1 activation.Oncogene · 2026Article
- Splicing isoforms associated with TGFβ-induced myofibroblast activation.BMC molecular and cell biology · 2026Article
- BCL-2 and BCL-xL in Cancer: Regulation, Function, and Therapeutic Targeting.International journal of molecular sciences · 2026Review
- Regulatory interplay between SR proteins governsRNA (New York, N.Y.) · 2024Article
- Stability-Based Proteomics for Investigation of Structured RNA-Protein Interactions.Analytical chemistry · 2024Article
- A dual role of RBM42 in modulating splicing and translation of CDKN1A/p21 during DNA damage response.Nature communications · 2023Article
- Alternative mRNA Splicing and Promising Therapies in Cancer.Biomolecules · 2023Review
- SRSF10 stabilizes CDC25A by triggering exon 6 skipping to promote hepatocarcinogenesis.Journal of experimental & clinical cancer research : CR · 2022Article
- The transcription factor c-Jun inhibits RBM39 to reprogram pre-mRNA splicing during genotoxic stress.Nucleic acids research · 2022Article
- Heterogeneous nuclear ribonucleoprotein A/B: an emerging group of cancer biomarkers and therapeutic targets.Cell death discovery · 2022Review
- 14-3-3 Proteins are Potential Regulators of Liquid-Liquid Phase Separation.Cell biochemistry and biophysics · 2022Review
- DNA Double-Strand Breaks as Pathogenic Lesions in Neurological Disorders.International journal of molecular sciences · 2022Review
- The aberrant upregulation of exon 10-inclusive SREK1 through SRSF10 acts as an oncogenic driver in human hepatocellular carcinoma.Nature communications · 2022Article
- hnRNP A1 in RNA metabolism regulation and as a potential therapeutic target.Frontiers in pharmacology · 2022Review
- RBM6 splicing factor promotes homologous recombination repair of double-strand breaks and modulates sensitivity to chemotherapeutic drugs.Nucleic acids research · 2021Article
- Replication stress signaling is a therapeutic target in myelodysplastic syndromes with splicing factor mutations.Haematologica · 2021Article
- SRSF10: an atypical splicing regulator with critical roles in stress response, organ development, and viral replication.RNA (New York, N.Y.) · 2021Review
- Aberrant Bcl-x splicing in cancer: from molecular mechanism to therapeutic modulation.Journal of experimental & clinical cancer research : CR · 2021Review
- A novel class of inhibitors that target SRSF10 and promote p53-mediated cytotoxicity on human colorectal cancer cells.NAR cancer · 2021Article
- Identification of SRSF10 as a regulator of SMN2 ISS-N1.Human mutation · 2021Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Little is known about how RNA binding proteins cooperate to control splicing, and how stress pathways reconfigure these assemblies to alter splice site selection. We have shown previously that SRSF10 plays an important role in the Bcl-x splicing response to DNA damage elicited by oxaliplatin in 293 cells. Here, RNA affinity assays using a portion of the Bcl-x transcript required for this response led to the recovery of the SRSF10-interacting protein 14-3-3ε and the Sam68-interacting protein hnRNP A1. Although SRSF10, 14-3-3ε, hnRNP A1/A2 and Sam68 do not make major contributions to the regulation of Bcl-x splicing under normal growth conditions, upon DNA damage they become important to activate the 5' splice site of pro-apoptotic Bcl-xS. Our results indicate that DNA damage reconfigures the binding and activity of several regulatory RNA binding proteins on the Bcl-x pre-mRNA. Moreover, SRSF10, hnRNP A1/A2 and Sam68 collaborate to drive the DNA damage-induced splicing response of several transcripts that produce components implicated in apoptosis, cell-cycle control and DNA repair. Our study reveals how the circuitry of splicing factors is rewired to produce partnerships that coordinate alternative splicing across processes crucial for cell fate.
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