ArticleOncogene2008
Snm1B/Apollo mediates replication fork collapse and S Phase checkpoint activation in response to DNA interstrand cross-links.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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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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Who cites it
42 citing papers in PubMed, 76 citations in OpenAlex.
- Mapping the genetic landscape of the DNA damage response with Cas12a-based combinatorial knockout screens.bioRxiv : the preprint server for biology · 2026Article
- Association of missense variant DCLRE1B rs3761936 with breast and cervical cancer risk-A case-control study.PloS one · 2025Article
- Structure and Function of SNM1 Family Nucleases.Advances in experimental medicine and biology · 2023Review
- Dual targeting of Saccharomyces cerevisiae Pso2 to mitochondria and the nucleus, and its functional relevance in the repair of DNA interstrand crosslinks.G3 (Bethesda, Md.) · 2022Article
- Inherited human Apollo deficiency causes severe bone marrow failure and developmental defects.Blood · 2022Article
- A phosphate binding pocket is a key determinant of exo- versus endo-nucleolytic activity in the SNM1 nuclease family.Nucleic acids research · 2021Article
- The SNM1A DNA repair nuclease.DNA repair · 2020Review
- Heat shock proteins and DNA repair mechanisms: an updated overview.Cell stress & chaperones · 2018Review
- SNM1B/Apollo in the DNA damage response and telomere maintenance.Oncotarget · 2017Review
- A role of human RNase P subunits, Rpp29 and Rpp21, in homology directed-repair of double-strand breaks.Scientific reports · 2017Article
- Review
- The Chemical Biology of Human Metallo-β-Lactamase Fold Proteins.Trends in biochemical sciences · 2016Review
- The structures of the SNM1A and SNM1B/Apollo nuclease domains reveal a potential basis for their distinct DNA processing activities.Nucleic acids research · 2015Article
- NUCKS1 is a novel RAD51AP1 paralog important for homologous recombination and genome stability.Nucleic acids research · 2015Article
- Emergence and evolutionary analysis of the human DDR network: implications in comparative genomics and downstream analyses.Molecular biology and evolution · 2014Article
- The SNM1B/APOLLO DNA nuclease functions in resolution of replication stress and maintenance of common fragile site stability.Human molecular genetics · 2013Article
- Telomere-end processing: mechanisms and regulation.Chromosoma · 2013Article
- Dna2 is involved in CA strand resection and nascent lagging strand completion at native yeast telomeres.The Journal of biological chemistry · 2013Article
- Artemis-dependent DNA double-strand break formation at stalled replication forks.Cancer science · 2013Article
- Telomere structure and telomerase in health and disease (review).International journal of oncology · 2012Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
The removal of DNA interstrand cross-links (ICLs) has proven to be notoriously complicated due to the involvement of multiple pathways of DNA repair, which include the Fanconi anemia/BRCA pathway, homologous recombination and components of the nucleotide excision and mismatch repair pathways. Members of the SNM1 gene family have also been shown to have a role in mediating cellular resistance to ICLs, although their precise function has remained elusive. Here, we show that knockdown of Snm1B/Apollo in human cells results in hypersensitivity to mitomycin C (MMC), but not to IR. We also show that Snm1B-deficient cells exhibit a defective S phase checkpoint in response to MMC, but not to IR, and this finding may account for the specific sensitivity to the cross-linking drug. Interestingly, although previous studies have largely implicated ATR as the major kinase activated in response to ICLs, we show that it is activation of the ATM-mediated checkpoint that is defective in Snm1B-deficient cells. The requirement for Snm1B in ATM checkpoint activation specifically after ICL damage is correlated with its role in promoting double-strand break formation, and thus replication fork collapse. Consistent with this result Snm1B was found to interact directly with Mus81-Eme1, an endonuclease previously implicated in fork collapse. In addition, we also show that Snm1B interacts with the Mre11-Rad50-Nbs1 (MRN) complex and with FancD2 further substantiating its role as a checkpoint/DNA repair protein.
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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.