@article{ETD,
      recid = {463},
      author = {de Graaf, Bendert},
      title = {Cellular response pathways to formaldehyde},
      publisher = {Oregon Health and Science University},
      school = {Ph.D.},
      address = {2009},
      number = {ETD},
      abstract = {DNA–protein crosslinks (DPCs) form after exposure to  agents such as formaldehyde, yet the pathways that repair  or tolerate these lesions are not fully defined. A  genome‑wide yeast deletion screen revealed that chronic  low‑dose formaldehyde toxicity is primarily mitigated by  homologous recombination, whereas acute high‑dose exposure  depends on nucleotide excision repair (NER). Findings  suggest that acute repair proceeds through NER‑dependent  single‑strand break intermediates without detectable  double‑strand breaks. Additional analyses show that  translesion synthesis acts as a backup pathway and that  Mre11 and Rad1 contribute independently to DPC tolerance.  These results highlight distinct pathway requirements for  chronic versus acute DPC exposure.},
      url = {http://digitalcollections.ohsu.edu/record/463},
      doi = {https://doi.org/10.6083/M41N7Z38},
}