Here, Wu et al. demonstrate that the DNA repair factor HMCES strongly suppresses deletions without significantly affecting other parameters of somatic hypermutation in mouse and human B cells, thereby facilitating the production of antigen-specific antibodies. Their findings lead to a novel model for the protection of Ig gene integrity during SHM in which abasic site cross-linking by HMCES intercedes at a critical juncture during processing of vulnerable gapped DNA intermediates by BER and MMR enzymes.
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机译:在这里,Wu 等人证明 DNA 修复因子 HMCES 强烈抑制缺失,而不会显着影响小鼠和人 B 细胞体细胞超突变的其他参数,从而促进抗原特异性抗体的产生。他们的发现导致了一种在 SHM 期间保护 Ig 基因完整性的新模型,其中 HMCES 的无碱基位点交联在 BER 和 MMR 酶加工脆弱的间隙 DNA 中间体的关键时刻介入。
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