ArticleGene2008
Splicing and splice factor SRp55 participate in the response to DNA damage by changing isoform ratios of target genes.
Article in Gene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Serine Starvation Modulates mRNA Splicing through Translational Inhibition of SRSF Proteins.Cancer research · 2026Article
- The Role of Interleukin-24 and Downstream Pathways in Inflammatory and Autoimmune Diseases.Cell biochemistry and biophysics · 2025Review
- SRSF6 balances mitochondrial-driven innate immune outcomes through alternative splicing of BAX.eLife · 2022Article
- Protein kinase R is an innate immune sensor of proteotoxic stress via accumulation of cytoplasmic IL-24.Science immunology · 2022Article
- Recent insights into apoptosis and toxic autophagy: The roles of MDA-7/IL-24, a multidimensional anti-cancer therapeutic.Seminars in cancer biology · 2020Review
- Role of MDA-7/IL-24 a Multifunction Protein in Human Diseases.Advances in cancer research · 2018Review
- MAD2γ, a novel MAD2 isoform, reduces mitotic arrest and is associated with resistance in testicular germ cell tumors.Cell cycle (Georgetown, Tex.) · 2016Article
- Mechanism of Action and Applications of Interleukin 24 in Immunotherapy.International journal of molecular sciences · 2016Review
- Dysregulation of splicing proteins in head and neck squamous cell carcinoma.Cancer biology & therapy · 2016Article
- JAK2 exon 14 skipping in patients with primary myelofibrosis: a minor splice variant modulated by the JAK2-V617F allele burden.PloS one · 2015Article
- Transcription elongation factor ELL2 drives Ig secretory-specific mRNA production and the unfolded protein response.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Autoantibodies to tumor-associated antigens as biomarkers in human hepatocellular carcinoma (HCC).Experimental hematology & oncology · 2013Article
- Time course changes of anti- and pro-apoptotic proteins in apigenin-induced genotoxicity.Chinese medicine · 2013Article
- Genotoxic stress modulates CDC25C phosphatase alternative splicing in human breast cancer cell lines.Molecular oncology · 2012Article
- Splice variants of mda-7/IL-24 differentially affect survival and induce apoptosis in U2OS cells.Cytokine · 2011Article
- Genotoxic stress causes the accumulation of the splicing regulator Sam68 in nuclear foci of transcriptionally active chromatin.Nucleic acids research · 2010Article
- High resolution analysis of the human transcriptome: detection of extensive alternative splicing independent of transcriptional activity.BMC genetics · 2009Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Alternative splicing is an important source of protein diversity, and is an established but not yet fully understood mechanism for gene regulation in higher eukaryotes. Its regulation is governed by a variety of mechanisms, including variation in the expression levels of splicing factors engaged in spliceosome formation. SRp55 is one of the most ubiquitous splicing factors and one that can be up-regulated by DNA damage in the absence of p53, and we had previously found that depletion of its activity increased resistance to DNA damage in p53-dependant manner. To assess its influence on the splicing patterns of genes involved in apoptosis, we performed splice-specific microarray analysis of cells treated with siRNA specific for this gene. This analysis, backed by RT-PCR verification, identified three genes, KSR1, ZAK and mda7/IL24, which are sensitive to SRp55 depletion. We also analyzed the splice patterns of apoptosis-related genes in p53-deficient U2OS cells following treatment with the genotoxic drug mitomycin C. This analysis revealed that DNA damage resulted in changes in splicing activity that modified the splicing pattern of Fas, a key pro-apoptotic, p53-inducible death receptor. Interestingly, this modification led to an enrichment of the anti-apoptotic soluble Fas isoform, and this secreted isoform was detected in the media surrounding cells subjected to DNA damage. These findings show that modulation of splicing activity in p53-deficient cells during the early response to sub-lethal DNA damage results in a change in the splicing of target genes, thus modifying the cellular response to genotoxic agents.
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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.