ArticleOncogene1999
Phosphorylation of the DNA repair protein APE/REF-1 by CKII affects redox regulation of AP-1.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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.
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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
37 citing papers in PubMed, 103 citations in OpenAlex.
- Contrasting roles of APE1 and APE2 in genome maintenance, cancer development, and therapeutic targeting.NAR cancer · 2025Review
- Post-translational modifications in DNA damage repair: mechanisms underlying temozolomide resistance in glioblastoma.Oncogene · 2025Review
- Cysteine Oxidation to Sulfenic Acid in APE1 Aids G-Quadruplex Binding While Compromising DNA Repair.ACS chemical biology · 2022Article
- CK2 and the Hallmarks of Cancer.Biomedicines · 2022Review
- Medulloblastoma and the DNA Damage Response.Frontiers in oncology · 2022Review
- Molecular Mechanisms Regulating the DNA Repair Protein APE1: A Focus on Its Flexible N-Terminal Tail Domain.International journal of molecular sciences · 2021Review
- Ref-1/APE1 as a Transcriptional Regulator and Novel Therapeutic Target in Pediatric T-cell Leukemia.Molecular cancer therapeutics · 2017Article
- Polyubiquitination of apurinic/apyrimidinic endonuclease 1 by Parkin.Molecular carcinogenesis · 2017Article
- Article
- Base Excision Repair, a Pathway Regulated by Posttranslational Modifications.Molecular and cellular biology · 2016Review
- Dynamic Regulation of APE1/Ref-1 as a Therapeutic Target Protein.Chonnam medical journal · 2016Review
- APE1/Ref-1 as an emerging therapeutic target for various human diseases: phytochemical modulation of its functions.Experimental & molecular medicine · 2014Review
- New perspectives on oxidized genome damage and repair inhibition by pro-oxidant metals in neurological diseases.Biomolecules · 2014Review
- Human apurinic/apyrimidinic endonuclease 1.Antioxidants & redox signaling · 2014Review
- Repair of oxidative DNA damage and cancer: recent progress in DNA base excision repair.Antioxidants & redox signaling · 2014Review
- Oxidative genome damage and its repair: implications in aging and neurodegenerative diseases.Mechanisms of ageing and development · 2012Review
- ATM-dependent downregulation of USP7/HAUSP by PPM1G activates p53 response to DNA damage.Molecular cell · 2012Article
- Oxidized base damage and single-strand break repair in mammalian genomes: role of disordered regions and posttranslational modifications in early enzymes.Progress in molecular biology and translational science · 2012Review
- S-glutathionylation of cysteine 99 in the APE1 protein impairs abasic endonuclease activity.Journal of molecular biology · 2011Article
- Ubiquitination of human AP-endonuclease 1 (APE1) enhanced by T233E substitution and by CDK5.Nucleic acids research · 2011Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The DNA repair protein apurinic endonuclease (APE/Ref-1) exerts several physiological functions such as cleavage of apurinic/apyrimidinic sites and redox regulation of the transcription factor AP-1, whose activation is part of the cellular response to DNA damaging treatments. Here we demonstrate that APE/Ref-1 is phosphorylated by casein kinase II (CKII). This was shown for both the recombinant APE/Ref-1 protein (Km=0.55 mM) and for APE/Ref-1 expressed in COS cells. Phosphorylation of APE/Ref-1 did not alter the repair activity of the enzyme, whereas it stimulated its redox capability towards AP-1, thus promoting DNA binding activity of AP-1. Inhibition of CKII mediated phosphorylation of APE/Ref-1 blocked mutagen-stimulated increase in AP-1 binding. It also abrogated the induction of c-Jun protein and rendered cells more sensitive to induced DNA damage. Thus, phosphorylation of APE/Ref-1 appears to be involved in regulating the different physiological activities of the enzyme. CKII mediated phosphorylation of APE/Ref-1 and concomitant increase in AP-1 binding activity appears to be a novel mechanism of cellular stress response, forcing transcription of AP-1 target gene(s) the product(s) of which may exert protective function.
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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.