ArticleNature communications2018
ZNF506-dependent positive feedback loop regulates H2AX signaling after DNA damage.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
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- RNA-binding protein ZCCHC4 promotes human cancer chemoresistance by disrupting DNA-damage-induced apoptosis.Signal transduction and targeted therapy · 2022Article
- Redox-sensitive iodinated polymersomes carrying histone deacetylase inhibitor as a dual-functional nano-radiosensitizer for enhanced radiotherapy of breast cancer.Drug delivery · 2021Article
- Histone H2A.X phosphorylation and Caspase-Initiated Chromatin Condensation in late-stage erythropoiesis.Epigenetics & chromatin · 2021Article
- 2D vanadium carbide MXenzyme to alleviate ROS-mediated inflammatory and neurodegenerative diseases.Nature communications · 2021Article
- Computational Tumor Infiltration Phenotypes Enable the Spatial and Genomic Analysis of Immune Infiltration in Colorectal Cancer.Frontiers in oncology · 2021Article
- The multi-functional eyes absent proteins.Critical reviews in biochemistry and molecular biology · 2020Review
- Reversible inhibitor of CRM1 sensitizes glioblastoma cells to radiation by blocking the NF-κB signaling pathway.Cancer cell international · 2020Article
- Knockdown of PKM2 enhances radiosensitivity of cervical cancer cells.Cancer cell international · 2019Article
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Cells respond to cytotoxic DNA double-strand breaks by recruiting repair proteins to the damaged site. Phosphorylation of the histone variant H2AX at S139 and Y142 modulate its interaction with downstream DNA repair proteins and their recruitment to DNA lesions. Here we report ATM-dependent ZNF506 localization to the lesion through MDC1 following DNA damage. ZNF506, in turn, recruits the protein phosphatase EYA, resulting in dephosphorylation of H2AX at Y142, which further facilitates the recruitment of MDC1 and other downstream repair factors. Thus, ZNF506 regulates the early dynamic signaling in the DNA damage response (DDR) pathway and controls progressive downstream signal amplification. Cells lacking ZNF506 or harboring mutations found in cancer patient samples are more sensitive to radiation, offering a potential new therapeutic option for cancers with mutations in this pathway. Taken together, these results demonstrate how the DDR pathway is orchestrated by ZNF506 to maintain genomic integrity.
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