Abstract
H2AX is required for genome stability. In response to DNA double-strand breaks (DSBs), H2AX is rapidly phosphorylated to form γH2AX foci, which mediate DNA repair and checkpoint signaling. This process is regulated by modifications and molecular interactions of H2AX. In addition, the rapid stabilization of H2AX in response to DSBs facilitates γH2AX foci formation. Although H2AX is markedly downregulated in many cellular states, γH2AX foci can still efficiently form upon DSB generation. Here, we review the regulation of H2AX in response to DSBs.
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