ArticleNucleic acids research2018
APE1 deficiency promotes cellular senescence and premature aging features.
Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 68 citations in OpenAlex.
- Apurinic/apyrimidinic endonuclease 1 prevents oxidative DNA damage in intestinal epithelial cells induced by genotoxic Escherichia coli NC101.Redox biology · 2026Article
- APE1 binds and processes abasic sites present in i-motif DNA and cooperates with PCBP1 in maintenance of telomeric stability.Nucleic acids research · 2026Article
- Structural basis for the mechanism and stability of the EEPD1 5' endonuclease.The Journal of biological chemistry · 2026Article
- Caloric restriction decelerates premature aging and cognitive decline in mice with deficient DNA repair.Communications biology · 2026Article
- FGF2 Enhances MSCs Secretome Therapy for Skin Photoaging by Delaying Senescence via iNAMPT/AMPK Signaling and Facilitating eNAMPT-Mediated Regenerative Crosstalk.Stem cell reviews and reports · 2026Article
- Contrasting roles of APE1 and APE2 in genome maintenance, cancer development, and therapeutic targeting.NAR cancer · 2025Review
- APE1 Attenuates ALK Tyrosine Kinase Inhibitors Sensitivity in NPM1-ALK Positive Anaplastic Large Cell Lymphoma.Cancer science · 2025Article
- APEX1-STAT3 signaling mediates the force-coordinated endothelial regeneration.Cellular and molecular life sciences : CMLS · 2025Article
- Real-Time, Light-Activated, and Multiplexed Monitoring of Base Excision Repair in Living Cells Using Chimeric d/l-DNA Molecular Beacons.ACS sensors · 2025Article
- Autophagy: The convergence point of aging and cancer.Biochemistry and biophysics reports · 2025Review
- Article
- From DNA Repair to Redox Signaling: The Multifaceted Role of APEX1 (Apurinic/Apyrimidinic Endonuclease 1) in Cardiovascular Health and Disease.International journal of molecular sciences · 2025Review
- Exploring the Potential of Malvidin and Echiodinin as Probable Antileishmanial Agents Through In Silico Analysis and In Vitro Efficacy.Molecules (Basel, Switzerland) · 2025Article
- Single-cell RNA sequencing reveals transcriptomic landscape and potential targets for human testicular ageing.Human reproduction (Oxford, England) · 2024Article
- APE1 inhibition enhances ferroptotic cell death and contributes to hepatocellular carcinoma therapy.Cell death and differentiation · 2024Article
- The crosstalk between telomeres and DNA repair mechanisms: an overview to mammalian somatic cells, germ cells, and preimplantation embryos.Journal of assisted reproduction and genetics · 2024Review
- 8-Oxoadenine: A «New» Player of the Oxidative Stress in Mammals?International journal of molecular sciences · 2024Review
- The APE1/REF-1 and the hallmarks of cancer.Molecular biology reports · 2024Review
- AP endonuclease 1: Biological updates and advances in activity analysis.Methods in enzymology · 2024Article
- Back-Up Base Excision DNA Repair in Human Cells Deficient in the Major AP Endonuclease, APE1.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Base excision repair (BER) handles many forms of endogenous DNA damage, and apurinic/apyrimidinic endonuclease 1 (APE1) is central to this process. Deletion of both alleles of APE1 (a.k.a. Apex1) in mice leads to embryonic lethality, and deficiency in cells can promote cell death. Unlike most other BER proteins, APE1 expression is inversely correlated with cellular senescence in primary human fibroblasts. Depletion of APE1 via shRNA induced senescence in normal human BJ fibroblasts, a phenotype that was not seen in counterpart cells expressing telomerase. APE1 knock-down in primary fibroblasts resulted in global DNA damage accumulation, and the induction of p16INK4a and p21WAF1 stress response pathways; the DNA damage response, as assessed by γ-H2AX, was particularly pronounced at telomeres. Conditional knock-out of Apex1 in mice at post-natal day 7/12 resulted in impaired growth, reduced organ size, and increased cellular senescence. The effect of Apex1 deletion at post-natal week 6 was less obvious, other than cellular senescence, until ∼8-months of age, when premature aging characteristics, such as hair loss and impaired wound healing, were seen. Low APE1 expression in patient cancer tissue also correlated with increased senescence. Our results point to a key role for APE1 in regulating cellular senescence and aging features, with telomere status apparently affecting the outcome.
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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.