ArticleFree radical biology & medicine2012
Nuclear depletion of apurinic/apyrimidinic endonuclease 1 (Ape1/Ref-1) is an indicator of energy disruption in neurons.
Article in Free radical biology & medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- Targeting the APE1 hub: integrating DNA repair and redox signaling for precision management of inflammation-associated diseases.Molecular biology reports · 2026Review
- 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
- MSC-Based Cell Therapy in Neurological Diseases: A Concise Review of the Literature in Pre-Clinical and Clinical Research.Biomolecules · 2024Review
- Artemisitene suppresses tumorigenesis by inducing DNA damage through deregulating c-Myc-topoisomerase pathway.Oncogene · 2018Article
- Oxidative stress stimulates invasive potential in rat C6 and human U-87 MG glioblastoma cells via activation and cross-talk between PKM2, ENPP2 and APE1 enzymes.Metabolic brain disease · 2018Article
- Neurotoxicity of cytarabine (Ara-C) in dorsal root ganglion neurons originates from impediment of mtDNA synthesis and compromise of mitochondrial function.Free radical biology & medicine · 2018Article
- Cisplatin Toxicity in Dorsal Root Ganglion Neurons Is Relieved by Meclizine via Diminution of Mitochondrial Compromise and Improved Clearance of DNA Damage.Molecular neurobiology · 2017Article
- An in vitro study ascertaining the role of HMetabolic brain disease · 2017Article
- The Emerging Role of GLP-1 Receptors in DNA Repair: Implications in Neurological Disorders.International journal of molecular sciences · 2017Review
- Augmentation of glycolytic metabolism by meclizine is indispensable for protection of dorsal root ganglion neurons from hypoxia-induced mitochondrial compromise.Free radical biology & medicine · 2016Article
- APE1/Ref-1 facilitates recovery of gray and white matter and neurological function after mild stroke injury.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- APE1, the DNA base excision repair protein, regulates the removal of platinum adducts in sensory neuronal cultures by NER.Mutation research · 2015Article
- Apurinic/apyrimidinic endonuclease 1 upregulation reduces oxidative DNA damage and protects hippocampal neurons from ischemic injury.Antioxidants & redox signaling · 2015Article
- Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress.Cellular and molecular life sciences : CMLS · 2014Review
- Neuroglobin mitigates mitochondrial impairments induced by acute inhalation of combustion smoke in the mouse brain.Inhalation toxicology · 2014Article
- GWAS in a box: statistical and visual analytics of structured associations via GenAMap.PloS one · 2014Article
- Overexpressed neuroglobin raises threshold for nitric oxide-induced impairment of mitochondrial respiratory activities and stress signaling in primary cortical neurons.Nitric oxide : biology and chemistry · 2013Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Apurinic/apyrimidinic endonuclease 1 (Ape1/Ref-1) is a multifunctional protein critical for cellular survival. Its involvement in adaptive survival responses includes key roles in redox sensing, transcriptional regulation, and repair of DNA damage via the base excision repair (BER) pathway. Ape1 is abundant in most cell types and central in integrating the first BER step catalyzed by different DNA glycosylases. BER is the main process for removal of oxidative DNA lesions in postmitotic brain cells, and after ischemic brain injury preservation of Ape1 coincides with neuronal survival, while its loss has been associated with neuronal death. Here, we report that in cultured primary neurons, diminution of cellular ATP by either oligomycin or H(2)O(2) is accompanied by depletion of nuclear Ape1, while other BER proteins are unaffected and retain their nuclear localization under these conditions. Importantly, while H(2)O(2) induces γH2AX phosphorylation, indicative of chromatin rearrangements in response to DNA damage, oligomycin does not. Furthermore, despite comparable diminution of ATP content, H(2)O(2) and oligomycin differentially affect critical parameters of mitochondrial respiration that ultimately determine cellular ATP content. Taken together, our findings demonstrate that in neurons, nuclear compartmentalization of Ape1 depends on ATP and loss of nuclear Ape1 reflects disruption of neuronal energy homeostasis. Energy crisis is a hallmark of stroke and other ischemic/hypoxic brain injuries. In vivo studies have shown that Ape1 deficit precedes neuronal loss in injured brain regions. Thus, our findings bring to light the possibility that energy failure-induced Ape1 depletion triggers neuronal death in ischemic brain injuries.
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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.