Broken DNA—be it a gap, a nick or a double strand break —is a hallmark of cancerous or aging cells. But once key kinases and their regulators detect DNA damage, a molecular cascade swings into action, triggering posttranscriptional changes in proteins that eventually spur enzymes, such as ligases, to repair the damage and facilitate further replication. Until recently, little was known about exactly how mammalian cells sense DNA damage and coordinate these responses and which molecules act to set things right.












