ArticleNucleic acids research2015
The COP9 signalosome is vital for timely repair of DNA double-strand breaks.
Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 44 citations in OpenAlex.
- Neddylation: from regulatory mechanisms to clinical implications in cancer.Journal of advanced research · 2026Review
- COP9 signalosome regulates EGFR and Notch signaling during myeloid-type progenitor cell fate decision in Drosophila.EMBO reports · 2026Article
- Sexual dimorphism in zebrafish liver proteins and implications for hepatic regeneration and diseases.Scientific reports · 2025Article
- PCAF-mediated acetylation regulates RAD51 dynamic localization on chromatin during HR repair.EMBO reports · 2025Article
- DoUBLing up: ubiquitin and ubiquitin-like proteases in genome stability.The Biochemical journal · 2024Review
- Advancements in colorectal cancer research: Unveiling the cellular and molecular mechanisms of neddylation (Review).International journal of oncology · 2024Review
- SMC5/6 Promotes Replication Fork Stability via Negative Regulation of the COP9 Signalosome.International journal of molecular sciences · 2024Article
- A supervised protein complex prediction method with network representation learning and gene ontology knowledge.BMC bioinformatics · 2022Article
- CRL4AOncogene · 2021Article
- Transcriptome network of the papillary thyroid carcinoma radiation marker CLIP2.Radiation oncology (London, England) · 2020Article
- The COP9 Signalosome: A Multi-DUB Complex.Biomolecules · 2020Review
- Duplication and divergence: New insights into AXR1 and AXL functions in DNA repair and meiosis.Scientific reports · 2020Article
- Interaction between NSMCE4A and GPS1 links the SMC5/6 complex to the COP9 signalosome.BMC molecular and cell biology · 2020Article
- CSNAP, the smallest CSN subunit, modulates proteostasis through cullin-RING ubiquitin ligases.Cell death and differentiation · 2020Article
- Beyond reversal: ubiquitin and ubiquitin-like proteases and the orchestration of the DNA double strand break repair response.Biochemical Society transactions · 2019Review
- CSN5A Subunit of COP9 Signalosome Temporally Buffers Response to Heat in Arabidopsis.Biomolecules · 2019Article
- Role of Cop9 Signalosome Subunits in the Environmental and Hormonal Balance of Plant.Biomolecules · 2019Review
- The CSN3 subunit of the COP9 signalosome interacts with the HD region of Sos1 regulating stability of this GEF protein.Oncogenesis · 2019Article
- Nuclear poly(A)-binding protein 1 is an ATM target and essential for DNA double-strand break repair.Nucleic acids research · 2018Article
- Analysis of RNA expression of normal and cancer tissues reveals high correlation of COP9 gene expression with respiratory chain complex components.BMC genomics · 2016Article
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 4 countries.
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Abstract
The DNA damage response is vigorously activated by DNA double-strand breaks (DSBs). The chief mobilizer of the DSB response is the ATM protein kinase. We discovered that the COP9 signalosome (CSN) is a crucial player in the DSB response and an ATM target. CSN is a protein complex that regulates the activity of cullin ring ubiquitin ligase (CRL) complexes by removing the ubiquitin-like protein, NEDD8, from their cullin scaffold. We find that the CSN is physically recruited to DSB sites in a neddylation-dependent manner, and is required for timely repair of DSBs, affecting the balance between the two major DSB repair pathways-nonhomologous end-joining and homologous recombination repair (HRR). The CSN is essential for the processivity of deep end-resection-the initial step in HRR. Cullin 4a (CUL4A) is recruited to DSB sites in a CSN- and neddylation-dependent manner, suggesting that CSN partners with CRL4 in this pathway. Furthermore, we found that ATM-mediated phosphorylation of CSN subunit 3 on S410 is critical for proper DSB repair, and that loss of this phosphorylation site alone is sufficient to cause a DDR deficiency phenotype in the mouse. This novel branch of the DSB response thus significantly affects genome stability.
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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.