BD Transduction Laboratories™ Purified Mouse Anti-Human XRCC4

DNA double-strand breaks (DSB) are generated during intrinsic eukaryotic DNA recombination events such as assembly of antigen receptor genes and meiotic and mitotic recombination.  DSB repair proteins are also required to repair breaks induced by extrinsic factors such as ionizing radiation and mutagenic chemicals.  DNA-PKcs, Ku70/Ku80, DNA ligase IV, and X-Ray Cross Complementation group 4 (XRCC4) are DSB proteins involved in both V(D)J recombination and DNA double-stranded break repair.  XRCC4 activates DNA ligase IV and cells deficient in XRCC4 inefficiently form coding joints and signal joints during V(D)J recombination.  XRCC4 contains a C-terminal nuclear localization sequence (NLS) and multiple phosphorylation sites, binds DNA, and is an effective substrate for DNA-PK.  Phosphorylation of XRCC4 has no effect on its interactions with DNA ligase IV or end-joining activity, but can inhibit its DNA binding activity.  Mice deficient in XRCC4 exhibit defects in lymphogenesis and apoptotic death of postmitotic neurons during neurogenesis.  Thus, XRCC4 is a ubiquitous protein involved in DNA end joining during DNA recombination and repair, which is critical for cell growth and survival.