Upon the occurrence of a DNA double-strand break, H2AX is rapidly phosphorylated at serine 139 by kinases such as ATM (ataxia-telangiectasia mutated) and ATR (ATM and Rad3-related). This phosphorylated form of H2AX is known as γ-H2AX (gamma-H2AX). The formation of γ-H2AX foci at the site of DNA damage facilitates the recruitment of DNA repair proteins and the assembly of repair complexes.
