Non-Homologous End Joining (NHEJ) DNA Repair Antibody Sampler Kit #76696

DNA double-strand breaks (DSBs) are potentially hazardous lesions that can be induced by ionizing radiation (IR), radiomimetic chemicals, or DNA replication inhibitors. Cells recognize and repair DSBs via two distinct but partly overlapping signaling pathways, non-homologous end joining (NHEJ) and homologous recombination (HR). DNA repair via the HR pathway is restricted to S and G2 phases of the cell cycle, while NHEJ can occur during any phase. NHEJ machinery is also utilized in V(D)J recombination, a process that generates diversity in immunoglobulin and T cell receptor genes. Defects in both pathways have been associated with human disease, including cancer (1).
DNA repair through the NHEJ pathway involves a core group of proteins that includes the Ku heterodimer (Ku70/Ku80), DNA-PKcs, DNA ligase IV, XRCC4, and XLF. XLF interacts with XRCC4 and promotes the ligation of DNA strands by DNA ligase IV and the ligase cofactor XRCC4. The ATP-dependent ligation of free DNA ends is the final step in the NHEJ repair pathway (2). DNA ligase IV and the endonuclease artemis suppress homologous recombination and promote NHEJ (3).