ArticleMolecular and cellular biology2000
Disruption of mouse SNM1 causes increased sensitivity to the DNA interstrand cross-linking agent mitomycin C.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 134 citations in OpenAlex.
- Precision medicine for atherosclerotic cardiovascular disease: Integrative genomics maps risk loci and AI-predicted functional consequences.Clinical and translational medicine · 2026Article
- DCLRE1B as a novel prognostic biomarker associated with immune infiltration: a pancancer analysis.Scientific reports · 2024Article
- SNM1A is crucial for efficient repair of complex DNA breaks in human cells.Nature communications · 2024Article
- DCLRE1B promotes tumor progression and predicts immunotherapy response through METTL3-mediated m6A modification in pancreatic cancer.BMC cancer · 2023Article
- Origin, Diversity, and Multiple Roles of Enzymes with Metallo-β-Lactamase Fold from Different Organisms.Cells · 2023Review
- 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
- PrimPol-mediated repriming facilitates replication traverse of DNA interstrand crosslinks.The EMBO journal · 2021Article
- Identification of Bioactive SNM1A Inhibitors.ACS omega · 2021Article
- Probing the Binding Requirements of Modified Nucleosides with the DNA Nuclease SNM1A.Molecules (Basel, Switzerland) · 2021Article
- The SNM1A DNA repair nuclease.DNA repair · 2020Review
- Genome-Wide SNP Discovery in Indigenous Cattle Breeds of South Africa.Frontiers in genetics · 2019Article
- Ubiquitylation at the Fork: Making and Breaking Chains to Complete DNA Replication.International journal of molecular sciences · 2018Review
- The role of ADP-ribosylation in regulating DNA interstrand crosslink repair.Journal of cell science · 2016Article
- Fan1 deficiency results in DNA interstrand cross-link repair defects, enhanced tissue karyomegaly, and organ dysfunction.Genes & development · 2016Article
- The structures of the SNM1A and SNM1B/Apollo nuclease domains reveal a potential basis for their distinct DNA processing activities.Nucleic acids research · 2015Article
- RPA inhibition increases replication stress and suppresses tumor growth.Cancer research · 2014Article
- XPF-ERCC1 acts in Unhooking DNA interstrand crosslinks in cooperation with FANCD2 and FANCP/SLX4.Molecular cell · 2014Article
- Evidence that the DNA endonuclease ARTEMIS also has intrinsic 5'-exonuclease activity.The Journal of biological chemistry · 2014Article
- A prototypical Fanconi anemia pathway in lower eukaryotes?Cell cycle (Georgetown, Tex.) · 2012Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA interstrand cross-links (ICLs) represent lethal DNA damage, because they block transcription, replication, and segregation of DNA. Because of their genotoxicity, agents inducing ICLs are often used in antitumor therapy. The repair of ICLs is complex and involves proteins belonging to nucleotide excision, recombination, and translesion DNA repair pathways in Escherichia coli, Saccharomyces cerevisiae, and mammals. We cloned and analyzed mammalian homologs of the S. cerevisiae gene SNM1 (PSO2), which is specifically involved in ICL repair. Human Snm1, a nuclear protein, was ubiquitously expressed at a very low level. We generated mouse SNM1(-/-) embryonic stem cells and showed that these cells were sensitive to mitomycin C. In contrast to S. cerevisiae snm1 mutants, they were not significantly sensitive to other ICL agents, probably due to redundancy in mammalian ICL repair and the existence of other SNM1 homologs. The sensitivity to mitomycin C was complemented by transfection of the human SNM1 cDNA and by targeting of a genomic cDNA-murine SNM1 fusion construct to the disrupted locus. We also generated mice deficient for murine SNM1. They were viable and fertile and showed no major abnormalities. However, they were sensitive to mitomycin C. The ICL sensitivity of the mammalian SNM1 mutant suggests that SNM1 function and, by implication, ICL repair are at least partially conserved between S. cerevisiae and mammals.
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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.