Error-Prone Mismatch and Base Excision DNA Repair in Somatic Hypermutation

Shanzhi Wang, Richard Chahwan, Lirong Wei, Matthew D. Scharff

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

The large repertoire of antibodies that is achieved through V(D)J recombination does not create antibodies that have sufficient affinity and broad enough specificity to protect against all toxins and pathogenic organisms. To create such antibodies, B cells somatically hypermutate the antibody variable regions to increase affinity and the Ig switch regions to express those mutated variable regions with each of the isotypes through class switch recombination. This article focuses on how somatic mutations generated by activation-induced deaminase in the variable and switch regions are extended by noncanonical error-prone mismatch and base excision repair.

Original languageEnglish (US)
Title of host publicationMolecular Immunology
PublisherElsevier Inc.
Pages126-133
Number of pages8
Volume2
ISBN (Print)9780080921525
DOIs
StatePublished - Apr 27 2016

Keywords

  • AID
  • Antibody diversification
  • Base excision DNA repair
  • Class switch recombination
  • DNA mismatch repair
  • Double-strand break
  • Error-prone polymerase
  • Germinal center
  • Hotspot
  • Somatic hypermutation
  • Variable regions

ASJC Scopus subject areas

  • Medicine(all)

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  • Cite this

    Wang, S., Chahwan, R., Wei, L., & Scharff, M. D. (2016). Error-Prone Mismatch and Base Excision DNA Repair in Somatic Hypermutation. In Molecular Immunology (Vol. 2, pp. 126-133). Elsevier Inc.. https://doi.org/10.1016/B978-0-12-374279-7.05015-3