ArticleFree radical biology & medicine2020
Arginine methylation of APE1 promotes its mitochondrial translocation to protect cells from oxidative damage.
Article in Free radical biology & medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Multi-Omics and Clinical Data Analyses of Protein Arginine Methyltransferases in Pan-Cancer and Colorectal Cancer.International journal of medical sciences · 2026Article
- Contrasting roles of APE1 and APE2 in genome maintenance, cancer development, and therapeutic targeting.NAR cancer · 2025Review
- PRMT1 in Health and Disease: Emerging Perspectives From Molecular Mechanisms to Therapeutic Strategies.MedComm · 2025Review
- Arginine methylation in cancer: mechanisms and therapeutic implications.Biomarker research · 2025Review
- Protein arginine methyltransferases as regulators of cellular stress.Experimental neurology · 2025Review
- The APE1/REF-1 and the hallmarks of cancer.Molecular biology reports · 2024Review
- Altered accumulation of hepatic mitochondrial antioxidant proteins with age and environmental heat stress.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Article
- ROS-Induced Mitochondrial Dysfunction in CD4 T Cells from ART-Controlled People Living with HIV.Viruses · 2023Article
- The Role of Protein Arginine Methyltransferases in DNA Damage Response.International journal of molecular sciences · 2022Review
- How Protein Methylation Regulates Steroid Receptor Function.Endocrine reviews · 2022Review
- Cellular pathways influenced by protein arginine methylation: Implications for cancer.Molecular cell · 2021Review
- Structure, Activity, and Function of PRMT1.Life (Basel, Switzerland) · 2021Review
- Molecular Mechanisms Regulating the DNA Repair Protein APE1: A Focus on Its Flexible N-Terminal Tail Domain.International journal of molecular sciences · 2021Review
- APE1/Ref-1 - One Target with Multiple Indications: Emerging Aspects and New Directions.Journal of cellular signaling · 2021Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Apurinic/apyrimidinic endonuclease 1 (APE1) is an essential multifunctional protein in mammals that plays critical roles in DNA repair and redox signaling within the cell. Impaired APE1 function or dysregulation is associated with disease susceptibility and poor cancer prognosis. Orchestrated regulatory mechanisms are crucial to ensure its function in a specific subcellular location at specific time. Here, we report arginine methylation as a post-translational modification (PTM) that regulates APE1 translocation to mitochondria in HeLa and HEK-293 cells. Protein arginine methyl-transferase 1 (PRMT1) was shown to methylate APE1 in vitro. Site-directed mutagenesis identified R301 as the major methylation site. We confirmed that APE1 is methylated in cells and that the R301K mutation significantly reduces its methylation. Baseline mitochondrial APE1 levels were low under standard culture conditions, but they could be induced by oxidative agents. Methylation-deficient APE1 showed reduced mitochondrial translocation. Methylation affected the interaction of APE1 with Tom20, translocase of the outer mitochondrial membrane. Methylation-deficient APE1 resulted in increased mitochondrial DNA damage and increased cytochrome c release after stimuli. These data suggest that methylation of APE1 promotes its mitochondrial translocation and protects cells from oxidative damage. This work describes a novel PTM regulation model of APE1 subcellular distribution through arginine methylation.
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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.