title: Push back to respond better: regulatory inhibition of the DNA double-strand break response.
abstract: Single DNA lesions such as DNA double-strand breaks (DSBs) can cause cell death or trigger genome rearrangements that have oncogenic potential, and so the pathways that mend and signal DNA damage must be highly sensitive but, at the same time, selective and reversible. When initiated, boundaries must be set to restrict the DSB response to the site of the lesion. The integration of positive and, crucially, negative control points involving post-translational modifications such as phosphorylation, ubiquitylation and acetylation is key for building fast, effective responses to DNA damage and for mitigating the impact of DNA lesions on genome integrity.
authors.affiliation: 1] The Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, 600 University Avenue, Toronto, Ontario M5G 1X5, Canada. [2] Present address: DNA Damage Response Laboratory, London Research Institute, Cancer Research UK, Clare Hall, South Mimms, London EN6 3LD, UK.
authors.forename: Stephanie
authors.initials: S
authors.lastname: Panier
authors.forename: Daniel
authors.initials: D
authors.lastname: Durocher
mesh_terms: D000107:Acetylation; D002843:Chromatin / Q000235:genetics*; D053903:DNA Breaks, Double-Stranded; D004249:DNA Damage; D053263:Gene Regulatory Networks; D042822:Genomic Instability; D006801:Humans; D010766:Phosphorylation; D015398:Signal Transduction; D054875:Ubiquitination
chemical_list: D002843:Chromatin