ArticleNature cell biology2010
The role of Cdk5-mediated apurinic/apyrimidinic endonuclease 1 phosphorylation in neuronal death.
Article in Nature cell biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed.
- Lewy body dementia promotion by air pollutants.Science (New York, N.Y.) · 2025Article
- Post-translational modifications in DNA damage repair: mechanisms underlying temozolomide resistance in glioblastoma.Oncogene · 2025Review
- Early oxidative stress and DNA damage in Aβ-burdened hippocampal neurons in an Alzheimer's-like transgenic rat model.Communications biology · 2024Article
- Phosphorylation of the Human DNA Glycosylase NEIL2 Is Affected by Oxidative Stress and Modulates Its Activity.Antioxidants (Basel, Switzerland) · 2023Article
- α-synucleinopathy exerts sex-dimorphic effects on the multipurpose DNA repair/redox protein APE1 in mice and humans.Progress in neurobiology · 2022Article
- Spatially resolved in vivo imaging of inflammation-associated mRNA via enzymatic fluorescence amplification in a molecular beacon.Nature biomedical engineering · 2022Article
- Activated or Impaired: An Overview of DNA Repair in Neurodegenerative Diseases.Aging and disease · 2022Article
- Insights into the Pathogenesis of Neurodegenerative Diseases: Focus on Mitochondrial Dysfunction and Oxidative Stress.International journal of molecular sciences · 2021Review
- Blockage of Drp1 phosphorylation at Ser579 protects neurons against AβMolecular medicine reports · 2021Article
- Post-translational modifications of CDK5 and their biological roles in cancer.Molecular biomedicine · 2021Review
- Arginine methylation of APE1 promotes its mitochondrial translocation to protect cells from oxidative damage.Free radical biology & medicine · 2020Article
- Cdk5-mediated Drp1 phosphorylation drives mitochondrial defects and neuronal apoptosis in radiation-induced optic neuropathy.Cell death & disease · 2020Article
- ZIKV Infection Induces DNA Damage Response and Alters the Proteome of Gastrointestinal Cells.Viruses · 2020Article
- Retrospective assessment of cyclin-dependent kinase 5 mRNA and protein expression and its association with patient survival in breast cancer.Journal of cellular and molecular medicine · 2020Article
- Contributions of DNA Damage to Alzheimer's Disease.International journal of molecular sciences · 2020Review
- Tyrosine Phosphorylation as a Widespread Regulatory Mechanism in Prokaryotes.Journal of bacteriology · 2019Review
- A mitotic CDK5-PP4 phospho-signaling cascade primes 53BP1 for DNA repair in G1.Nature communications · 2019Article
- AP endonuclease 1 (Apex1) influences brain development linking oxidative stress and DNA repair.Cell death & disease · 2019Article
- Low dose dinaciclib enhances doxorubicin-induced senescence in myeloma RPMI8226 cells by transformation of the p21 and p16 pathways.Oncology letters · 2018Article
- Curcumin revitalizes Amyloid beta (25-35)-induced and organophosphate pesticides pestered neurotoxicity in SH-SY5Y and IMR-32 cells via activation of APE1 and Nrf2.Metabolic brain disease · 2017Article
6 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors.
Funding
Abstract
Accumulating evidence suggests that deregulated cyclin-dependent kinase 5 (Cdk5) plays a critical part in neuronal death. However, the pathogenic targets of Cdk5 are not fully defined. Here we demonstrate that the Cdk5 activator p35 interacts directly with apurinic/apyrimidinic endonuclease 1 (Ape1), a protein crucial for base excision repair (BER) following DNA damage. Cdk5 complexes phosphorylate Ape1 at Thr 232 and thereby reduces its apurinic/apyrimidinic (AP) endonuclease activity. Ape1 phosphorylation is dependent on Cdk5 in in vitro and in vivo. The reduced endonuclease activity of phosphorylated Ape1 results in accumulation of DNA damage and contributes to neuronal death. Overexpression of Ape1(WT) and Ape1(T232A), but not the phosphorylation mimic Ape1(T232E), protects neurons against MPP(+)/MPTP. Loss of Ape1 sensitizes neurons to death. Importantly, increased phosphorylated Ape1 was also observed in post-mortem brain tissue from patients with Parkinson's and Alzheimer's diseases, suggesting a potential link between Ape1 phosphorylation and the pathogenesis of neurodegenerative diseases.
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