ArticleOncogene2019
K120R mutation inactivates p53 by creating an aberrant splice site leading to nonsense-mediated mRNA decay.
Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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
13 citing papers in PubMed, 21 citations in OpenAlex.
- Splice-altering TP53 missense mutations as drivers of dysfunction and targets for RNA-based therapy.Stem cell research & therapy · 2026Article
- Antisense-mediated splicing correction as a therapeutic approach for p53 K120R mutation.BMB reports · 2024Article
- Cell fate regulation governed by p53: Friends or reversible foes in cancer therapy.Cancer communications (London, England) · 2024Review
- New Germline TP53 Variant Detected After Radiotherapy-Induced Angiosarcoma of the Chest Wall in a Previously Treated Breast Cancer Patient: A Case Report and Review of Li-Fraumeni Syndrome and Radiotherapy-Induced Sarcoma.Case reports in oncological medicine · 2024Article
- An Ethanol Extract ofNutrients · 2023Article
- Advances in Gene Therapy Techniques to TreatBiomolecules · 2022Review
- Differential Transcriptional Regulation of Polymorphic p53 Codon 72 in Metabolic Pathways.International journal of molecular sciences · 2021Article
- Luteolin Induces Selective Cell Death of Human Pluripotent Stem Cells.Biomedicines · 2020Article
- Regulating tumor suppressor genes: post-translational modifications.Signal transduction and targeted therapy · 2020Review
- Elimination of Teratogenic Human Induced Pluripotent Stem Cells by Bee Venom via Calcium-Calpain Pathway.International journal of molecular sciences · 2020Article
- Prunellae Spica Extract Suppresses Teratoma Formation of Pluripotent Stem Cells through p53-Mediated Apoptosis.Nutrients · 2020Article
- Two Novel Rare Strongly Linked Missense SNPs (P27R and A85G) Within theFrontiers in veterinary science · 2020Article
- Retroelement Insertion in a CRISPR/Cas9 Editing Site in the Early Embryo Intensifies Genetic Mosaicism.Frontiers in cell and developmental biology · 2019Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The point mutation that substitutes lysine with arginine at position 120 of human p53 has been characterized as a missense mutation. The K120R mutation renders the p53 protein disabled for acetylation and, as a result, defective for apoptotic function, which provides a mechanistic link between the missense mutation and tumorigenesis. However, we noticed the failures of tumorigenesis in mice with the mutation, and of the related studies to notice that it has arbitrarily reflected in amino acid change through a sequence modification (AGA) of the original tumor mutation (AGG) by codon degeneracy. Unlike this modified version, we also discovered a novel splicing site the original mutation, TP53 c.359A>G, may induce. Using a human induced pluripotent stem cell line that was engineered to be homozygous for the original mutation, we here identified that the accidental splicing site generates a defective transcript variant with a frame-shifted premature termination codon which is subjected to nonsense-mediated mRNA decay. The authentic splicing still occurs but in extremely low amounts. Taken together, this mutation causes depletion of cellular p53 via defective mRNA, suggesting a new link to tumorigenesis.
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Registered trials
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