Cells have evolved sophisticated mechanisms to detect and repair DSBs. Key players in the detection process include proteins such as ATM (Ataxia Telangiectasia Mutated) and ATR (ATM and Rad3-related), which recognize the DNA damage and initiate a signaling cascade. The presence of DSBs is also marked by the phosphorylation of the histone variant H2AX, forming γ-H2AX foci at the site of the break, which can be visualized using immunofluorescence techniques.
