ArticleNucleic acids research2013
UV-triggered p21 degradation facilitates damaged-DNA replication and preserves genomic stability.
Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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.
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.
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Who cites it
36 citing papers in PubMed, 50 citations in OpenAlex.
- Zfp36l1 Inhibits DNA Damage by Regulating p21-E2F1-Rad51 Signaling During Myogenic Differentiation.International journal of molecular sciences · 2026Article
- Endogenous p21 levels protect genomic stability by suppressing both excess and restrained nascent DNA syntheses.Science advances · 2025Article
- Versatile enhancement of the killing potential of anti-cancer agents achieved by peptide mimetics of the PCNA interface towards specialized DNA polymerases.Cell death & disease · 2025Article
- Human CST complex restricts excessive PrimPol repriming upon UV induced replication stress by suppressing p21.Nucleic acids research · 2024Article
- The levels of p53 govern the hierarchy of DNA damage tolerance pathway usage.Nucleic acids research · 2024Article
- Correction: Chromosomal Integrity after UV Irradiation Requires FANCD2-Mediated Repair of Double Strand Breaks.PLoS genetics · 2023Article
- Polymerase iota (Pol ι) prevents PrimPol-mediated nascent DNA synthesis and chromosome instability.Science advances · 2023Article
- Revisiting the Function of p21International journal of molecular sciences · 2022Review
- Impact of the interplay between stemness features, p53 and pol iota on replication pathway choices.Nucleic acids research · 2021Article
- Inverse and reciprocal regulation of p53/p21 and Bmi-1 modulates vasculogenic differentiation of dental pulp stem cells.Cell death & disease · 2021Article
- Regulation of DNA Replication Licensing and Re-Replication by Cdt1.International journal of molecular sciences · 2021Review
- Targeting Non-Oncogene Addiction for Cancer Therapy.Biomolecules · 2021Review
- Characterization of Molecular Subtypes in Head and Neck Squamous Cell Carcinoma With Distinct Prognosis and Treatment Responsiveness.Frontiers in cell and developmental biology · 2021Article
- Review
- Stress-induced changes in CARF expression determine cell fate to death, survival, or malignant transformation.Cell stress & chaperones · 2020Article
- Multiple interaction nodes define the postreplication repair response to UV-induced DNA damage that is defective in melanomas and correlated with UV signature mutation load.Molecular oncology · 2020Article
- Article
- Direct binding of Cdt2 to PCNA is important for targeting the CRL4Life science alliance · 2018Article
- Chromatin modifiers Mdm2 and RNF2 prevent RNA:DNA hybrids that impair DNA replication.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- 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
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Although many genotoxic treatments upregulate the cyclin kinase inhibitor p21, agents such as UV irradiation trigger p21 degradation. This suggests that p21 blocks a process relevant for the cellular response to UV. Here, we show that forced p21 stabilization after UV strongly impairs damaged-DNA replication, which is associated with permanent deficiencies in the recruitment of DNA polymerases from the Y family involved in translesion DNA synthesis), with the accumulation of DNA damage markers and increased genomic instability. Remarkably, such noxious effects disappear when disrupting the proliferating cell nuclear antigen (PCNA) interacting motif of stable p21, thus suggesting that the release of PCNA from p21 interaction is sufficient to allow the recruitment to PCNA of partners (such as Y polymerases) relevant for the UV response. Expression of degradable p21 only transiently delays early replication events and Y polymerase recruitment after UV irradiation. These temporary defects disappear in a manner that correlates with p21 degradation with no detectable consequences on later replication events or genomic stability. Together, our findings suggest that the biological role of UV-triggered p21 degradation is to prevent replication defects by facilitating the tolerance of UV-induced DNA lesions.
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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.