Simone Petersen

TL;DR: Higher order chromatin structure presents a barrier to the recognition and repair of DNA damage, and H2AX is critical for facilitating the assembly of specific DNA-repair complexes on damaged DNA.

TL;DR: It is reported that the Nijmegen breakage syndrome protein and phosphorylated H2A histone family member X (γ-H2AX) form nuclear foci at the Ch region in the G1 phase of the cell cycle in cells undergoing CSR, and that switching is impaired in H2AX-/- mice.

TL;DR: The results indicate that the complex phenotypes observed in NBS patients and cell lines may not result from a complete inactivation of NBS1 but may instead result from hypomorphic truncation mutations compatible with cell viability.

TL;DR: Mice deficient in both a nonhomologous end joining (NHEJ) DNA repair protein and the p53 tumor suppressor develop lymphomas at an early age harboring amplification of an IgH/c-myc fusion, report that these chromosomal rearrangements are initiated by a recombination activating gene (RAG)-induced DNA cleavage.