ArticleNucleic acids research2014
ARF induction in response to DNA strand breaks is regulated by PARP1.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 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
21 citing papers in PubMed, 54 citations in OpenAlex.
- SIRT1 as a masterful reciprocal regulator of molecular mechanisms and signaling pathways involved in tumor growth and expansion.Clinical and experimental medicine · 2025Review
- Crosstalk between BER and NHEJ in XRCC4-Deficient Cells Depending on hTERT Overexpression.International journal of molecular sciences · 2024Article
- Telomeres and SIRT1 as Biomarkers of Gamete Oxidative Stress, Fertility, and Potential IVF Outcome.International journal of molecular sciences · 2024Review
- Ketone Bodies and SIRT1, Synergic Epigenetic Regulators for Metabolic Health: A Narrative Review.Nutrients · 2022Review
- The Role of HDACs in the Response of Cancer Cells to Cellular Stress and the Potential for Therapeutic Intervention.International journal of molecular sciences · 2022Review
- Precise Diabetic Wound Therapy: PLS Nanospheres Eliminate Senescent Cells via DPP4 Targeting and PARP1 Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- The NUCKS1-SKP2-p21/p27 axis controls S phase entry.Nature communications · 2021Article
- SIRT1 regulates the phosphorylation and degradation of P27 by deacetylating CDK2 to promote T-cell acute lymphoblastic leukemia progression.Journal of experimental & clinical cancer research : CR · 2021Article
- Non-Canonical Functions of the ARF Tumor Suppressor in Development and Tumorigenesis.Biomolecules · 2021Review
- A unified model for the G1/S cell cycle transition.Nucleic acids research · 2020Review
- Persistent DNA damage triggers activation of the integrated stress response to promote cell survival under nutrient restriction.BMC biology · 2020Article
- The Role of SIRT1 on DNA Damage Response and Epigenetic Alterations in Cancer.International journal of molecular sciences · 2019Review
- Interplay between base excision repair protein XRCC1 and ALDH2 predicts overall survival in lung and liver cancer patients.Cellular oncology (Dordrecht, Netherlands) · 2018Article
- Article
- Modulation of proteostasis counteracts oxidative stress and affects DNA base excision repair capacity in ATM-deficient cells.Nucleic acids research · 2017Article
- Differing tumor-suppressor functions of Arf and p53 in murine basal cell carcinoma initiation and progression.Oncogene · 2017Article
- Review
- p53 coordinates base excision repair to prevent genomic instability.Nucleic acids research · 2016Article
- Cells deficient in base-excision repair reveal cancer hallmarks originating from adjustments to genetic instability.Nucleic acids research · 2015Article
- Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The ARF tumour suppressor protein, the gene of which is frequently mutated in many human cancers, plays an important role in the cellular stress response by orchestrating up-regulation of p53 protein and consequently promoting cell-cycle delay. Although p53 protein function has been clearly linked to the cellular DNA damage response, the role of ARF protein in this process is unclear. Here, we report that arf gene transcription is induced by DNA strand breaks (SBs) and that ARF protein accumulates in response to persistent DNA damage. We discovered that poly(ADP-ribose) synthesis catalysed by PARP1 at the sites of unrepaired SBs activates ARF transcription through a protein signalling cascade, including the NAD(+)-dependent deacetylase SIRT1 and the transcription factor E2F1. Our data suggest that poly(ADP-ribose) synthesis at the sites of SBs initiates DNA damage signal transduction by reducing the cellular concentration of NAD(+), thus down-regulating SIRT1 activity and consequently activating E2F1-dependent ARF transcription. Our findings suggest a vital role for ARF in DNA damage signalling, and furthermore explain the critical requirement for ARF inactivation in cancer cells, which are frequently deficient in DNA repair and accumulate DNA damage.
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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.