ArticleCancers2021
DNA-Damage-Induced Alternative Splicing of p53.
Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 16 citations in OpenAlex.
- A post-translational regulatory map of chronic antigen-driven human T cell dysfunction.bioRxiv : the preprint server for biology · 2026Article
- From molecular damage to regulatory constraint: epigenetic and metabolic limits of cellular plasticity in aging.Frontiers in aging · 2026Review
- Biology of p53 protein isoforms and their significance in hematological malignancies.Frontiers in oncology · 2026Review
- Alternative Splicing in Tumorigenesis and Cancer Therapy.Biomolecules · 2025Review
- Alternative Splicing: Emerging Roles in Anti-Aging Strategies.Biomolecules · 2025Review
- Decoding the general role of tRNA queuosine modification in eukaryotes.Scientific reports · 2025Article
- Advances on the Role of Ferroptosis in Ionizing Radiation Response.Current pharmaceutical biotechnology · 2024Review
- Participation of ATM, SMG1, and DDX5 in a DNA Damage-Induced Alternative Splicing Pathway.Radiation research · 2023Article
- Article
- A Novel Role of SMG1 in Cholesterol Homeostasis That Depends Partially on p53 Alternative Splicing.Cancers · 2022Article
- Cytoplasmic p53β Isoforms Are Associated with Worse Disease-Free Survival in Breast Cancer.International journal of molecular sciences · 2022Article
- Editorial: Advances in wild type and mutant p53 research in cancer.Frontiers in molecular biosciences · 2022Article
- Alveolar type 2 epithelial cell senescence and radiation-induced pulmonary fibrosis.Frontiers in cell and developmental biology · 2022Review
- Genome-Wide RNAi Screening Identifies Novel Pathways/Genes Involved in Oxidative Stress and Repurposable Drugs to Preserve Cystic Fibrosis Airway Epithelial Cell Integrity.Antioxidants (Basel, Switzerland) · 2021Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Cellular responses to DNA damage and other stresses are important determinants of mutagenesis and impact the development of a wide range of human diseases. TP53 is highly mutated in human cancers and plays an essential role in stress responses and cell fate determination. A central dogma of p53 induction after DNA damage has been that the induction results from a transient increase in the half-life of the p53 protein. Our laboratory recently demonstrated that this long-standing paradigm is an incomplete picture of p53 regulation by uncovering a critical role for protein translational regulation in p53 induction after DNA damage. These investigations led to the discovery of a DNA-damage-induced alternative splicing (AS) pathway that affects p53 and other gene products. The damage-induced AS of p53 pre-mRNA generates the beta isoform of p53 (p53β) RNA and protein, which is specifically required for the induction of cellular senescence markers after ionizing irradiation (IR). In an attempt to elucidate the mechanisms behind the differential regulation and apparent functional divergence between full-length (FL) p53 and the p53β isoform (apoptosis versus senescence, respectively), we identified the differential transcriptome and protein interactome between these two proteins that may result from the unique 10-amino-acid tail in p53β protein.
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Identifiers
What OpenQuestion holds
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.