ArticleDNA repair2014
ATMIN is required for the ATM-mediated signaling and recruitment of 53BP1 to DNA damage sites upon replication stress.
Article in DNA repair, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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
23 citing papers in PubMed, 33 citations in OpenAlex.
- The role of HECT-type E3 ubiquitin ligases in DNA damage response and repair.Cell death discovery · 2025Review
- 53BP1-the 'Pandora's box' of genome integrity.DNA repair · 2024Review
- Large-scale copy number alterations are enriched for synthetic viability in BRCA1/BRCA2 tumors.Genome medicine · 2024Article
- Osteosarcoma patient with Li-Fraumeni syndrome: the first case report in Vietnam.Frontiers in oncology · 2024Article
- R-Loop-Associated Genomic Instability and Implication of WRN and WRNIP1.International journal of molecular sciences · 2022Review
- Chronic exposure of humans to high level natural background radiation leads to robust expression of protective stress response proteins.Scientific reports · 2021Article
- Prognostic Signatures of Alternative Splicing Events in Esophageal Carcinoma Based on TCGA Splice-Seq Data.Frontiers in oncology · 2021Article
- The DNA damage response links human squamous proliferation with differentiation.The Journal of cell biology · 2020Article
- Checkpoint Defects Elicit a WRNIP1-Mediated Response to Counteract R-Loop-Associated Genomic Instability.Cancers · 2020Article
- An emerging regulatory network of NHEJ via DYNLL1-mediated 53BP1 redistribution.Annals of translational medicine · 2019Article
- ATM pathway activation limits R-loop-associated genomic instability in Werner syndrome cells.Nucleic acids research · 2019Article
- PPARγ Interaction with UBR5/ATMIN Promotes DNA Repair to Maintain Endothelial Homeostasis.Cell reports · 2019Article
- Around and beyond 53BP1 Nuclear Bodies.International journal of molecular sciences · 2017Review
- Article
- Dormant origins as a built-in safeguard in eukaryotic DNA replication against genome instability and disease development.DNA repair · 2017Review
- Genetic variants associated with mosaic Y chromosome loss highlight cell cycle genes and overlap with cancer susceptibility.Nature genetics · 2017Article
- The role of WRNIP1 in genome maintenance.Cell cycle (Georgetown, Tex.) · 2017Review
- Review
- MRNIP/C5orf45 Interacts with the MRN Complex and Contributes to the DNA Damage Response.Cell reports · 2016Article
- Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Unresolved replication intermediates can block the progression of replication forks and become converted into DNA lesions, hence exacerbating genomic instability. The p53-binding protein 1 (53BP1) forms nuclear bodies at sites of unrepaired DNA lesions to shield these regions against erosion, in a manner dependent on the DNA damage kinase ATM. The molecular mechanism by which ATM is activated upon replicative stress to localize the 53BP1 protection complex is unknown. Here we show that the ATM-INteracting protein ATMIN (also known as ASCIZ) is partially required for 53BP1 localization upon replicative stress. Additionally, we demonstrate that ATM activation is impaired in cells lacking ATMIN and we define that ATMIN is required for initiating ATM signaling following replicative stress. Furthermore, loss of ATMIN leads to chromosomal segregation defects. Together these data reveal that chromatin integrity depends on ATMIN upon exposure to replication-induced stress.
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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.