Cell-cycle-specific regulator of classical non-homologous end joining (NHEJ) of DNA double-strand break (DSB) repair, which can act both as an activator or inhibitor of NHEJ, depending on the cell cycle phase (, ). Acts as a regulator of DNA repair pathway choice by specifically inhibiting classical NHEJ during the S and G2 phases, thereby promoting error-free repair by homologous recombination during cell cycle phases when sister chromatids are present . Preferentially protects single-stranded overhangs at break sites by inhibiting classical NHEJ, thereby creating a local environment that favors homologous recombination . Acts via interaction with XRCC5/Ku80 and XRCC6/Ku70 . In contrast, acts as an activator of NHEJ during G1 phase of the cell cycle: promotes classical NHEJ in G1 phase cells via multivalent interactions that increase the affinity of DNA damage response proteins for DSB-associated chromatin. Also involved in immunoglobulin V(D)J recombination (By similarity). May also act as an indirect regulator of proteasome (By similarity).
Subcellular locations: Cytoplasm, Nucleus, Chromosome
Nuclear localization may depend upon interaction with XRCC5/Ku80 and XRCC6/Ku70 heterodimer . Localizes to DNA damage sites .
Subcellular locations: Cytoplasm
Some nuclear localization may be due to passive diffusion.
Subcellular locations: Cytoplasm, Nucleus
Nuclear localization may depend upon interaction with XRCC5/Ku80 and XRCC6/Ku70 heterodimer and increases upon etoposide treatment.