APE1- And APE2-dependent DNA breaks in immunoglobulin class switch recombination

Jeroen E.J. Guikema, Erin K. Linehan, Daisuke Tsuchimoto, Yusaku Nakabeppu, Phyllis R. Strauss, Janet Stavnezer, Carol E. Schrader

研究成果: ジャーナルへの寄稿学術誌査読

129 被引用数 (Scopus)

抄録

Antibody class switch recombination (CSR) occurs by an intrachromosomal deletion requiring generation of double-stranded breaks (DSBs) in switch-region DNA. The initial steps in DSB formation have been elucidated, involving cytosine deamination by activation-induced cytidine deaminase and generation of abasic sites by uracil DNA glycosylase. However, it is not known how abasic sites are converted into single-stranded breaks and, subsequently, DSBs. Apurinic/apyrimidinic endonuclease (APE) efficiently nicks DNA at abasic sites, but it is unknown whether APE participates in CSR. We address the roles of the two major mammalian APEs, APE1 and APE2, in CSR. APE1 deficiency causes embryonic lethality in mice; we therefore examined CSR and DSBs in mice deficient in APE2 and haploinsufficient for APE1. We show that both APE1 and APE2 function in CSR, resulting in the DSBs necessary for CSR and thereby describing a novel in vivo function for APE2. JEM

本文言語英語
ページ(範囲)3017-3026
ページ数10
ジャーナルJournal of Experimental Medicine
204
12
DOI
出版ステータス出版済み - 11月 26 2007

!!!All Science Journal Classification (ASJC) codes

  • 免疫アレルギー学
  • 免疫学

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