Ziqiang Li

TL;DR: The biochemical mechanism and regulation of SHM and CSR are the topic of this review and are largely targeted to the Ig genes, but their targeting to other genes causes many of the B-cell lymphomas in mice and humans.

TL;DR: It is shown that mice mutant for exonuclease 1 (Exo1), which participates in DNA mismatch repair (MMR), have decreased CSR and changes in the characteristics of SHM similar to those previously observed in mice Mutant for the MMR protein Msh2, which is the first exo1 shown to be involved in SHM and CSR.

TL;DR: The data suggest that MutS homologues Msh2, Msh3, and Msh6 play overlapping and distinct roles during antibody diversification processes during somatic hypermutation and CSR.

TL;DR: It is shown that, similar to Msh2−/− mice, SHM in Msh 2G674A mice is biased toward G-C mutations, however, CSR is partially reduced, and switch junctions are more similar to those of postmeiotic segregation 2−/+ mice than to MSh2− /− mice.

TL;DR: It is found that V regions that undergo somatic hypermutation were enriched in short patches of ssDNA, rather than R loops, on both the coding and noncoding strands, and regions of DNA that are targets of SHM assemble protein–DNA complexes in which ssDNA is exposed, making it accessible to AID.