ArticleNucleic acids research2010
CK2 phosphorylation-dependent interaction between aprataxin and MDC1 in the DNA damage response.
Article in Nucleic acids research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 61 citations in OpenAlex.
- Approach to Oculomotor Apraxia: A Syndromic Approach to Genetic Causes.Cerebellum (London, England) · 2025Review
- Dysfunctional copper homeostasis inRedox biochemistry and chemistry · 2024Article
- The regulatory subunits of CK2 complex mediate DNA damage response and virulence in Candida Glabrata.BMC microbiology · 2023Article
- Targeting CK2-mediated phosphorylation of p53R2 sensitizes BRCA-proficient cancer cells to PARP inhibitors.Oncogene · 2023Article
- APTX acts in DNA double-strand break repair in a manner distinct from XRCC4.Journal of radiation research · 2023Article
- Species variations in XRCC1 recruitment strategies for FHA domain-containing proteins.DNA repair · 2022Article
- Discovery of Novel Dual-Target Inhibitor of Bromodomain-Containing Protein 4/Casein Kinase 2 Inducing Apoptosis and Autophagy-Associated Cell Death for Triple-Negative Breast Cancer Therapy.Journal of medicinal chemistry · 2021Article
- Hybrid Drugs-A Strategy for Overcoming Anticancer Drug Resistance?Molecules (Basel, Switzerland) · 2021Review
- Phosphopeptide interactions of the Nbs1 N-terminal FHA-BRCT1/2 domains.Scientific reports · 2021Article
- Xeroderma Pigmentosum C: A Valuable Tool to Decipher the Signaling Pathways in Skin Cancers.Oxidative medicine and cellular longevity · 2021Review
- Synergistic Interactions of 5-Fluorouracil with Inhibitors of Protein Kinase CK2 Correlate with p38 MAPK Activation and FAK Inhibition in the Triple-Negative Breast Cancer Cell Line.International journal of molecular sciences · 2020Article
- DNA damage response signaling pathways and targets for radiotherapy sensitization in cancer.Signal transduction and targeted therapy · 2020Review
- Pathway Analysis of Fucoidan Activity Using a Yeast Gene Deletion Library Screen.Marine drugs · 2019Article
- Signaling Pathways, Chemical and Biological Modulators of Nucleotide Excision Repair: The Faithful Shield against UV Genotoxicity.Oxidative medicine and cellular longevity · 2019Review
- Molecular Signaling in Response to Charged Particle Exposures and its Importance in Particle Therapy.International journal of particle therapy · 2018Review
- Characterization of the APLF FHA-XRCC1 phosphopeptide interaction and its structural and functional implications.Nucleic acids research · 2017Article
- Complementation of aprataxin deficiency by base excision repair enzymes in mitochondrial extracts.Nucleic acids research · 2017Article
- Oxidative DNA double strand breaks and autophagy in the antitumor effect of sterically hindered platinum(II) complexes in NSCLCs.Oncotarget · 2017Article
- Neurological disorders associated with DNA strand-break processing enzymes.Mechanisms of ageing and development · 2017Review
- Predicting CK2 beta-dependent substrates using linear patterns.Biochemistry and biophysics reports · 2015Article
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 5 countries.
Funding
Abstract
Aprataxin, defective in the neurodegenerative disorder ataxia oculomotor apraxia type 1, resolves abortive DNA ligation intermediates during DNA repair. Here, we demonstrate that aprataxin localizes at sites of DNA damage induced by high LET radiation and binds to mediator of DNA-damage checkpoint protein 1 (MDC1/NFBD1) through a phosphorylation-dependent interaction. This interaction is mediated via the aprataxin FHA domain and multiple casein kinase 2 di-phosphorylated S-D-T-D motifs in MDC1. X-ray structural and mutagenic analysis of aprataxin FHA domain, combined with modelling of the pSDpTD peptide interaction suggest an unusual FHA binding mechanism mediated by a cluster of basic residues at and around the canonical pT-docking site. Mutation of aprataxin FHA Arg29 prevented its interaction with MDC1 and recruitment to sites of DNA damage. These results indicate that aprataxin is involved not only in single strand break repair but also in the processing of a subset of double strand breaks presumably through its interaction with MDC1.
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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.