Lee Gregory S, Brandt Vicky L, Roth David B
Skirball Institute of Biomolecular Medicine, Department of Pathology, New York University School of Medicine, New York, New York 10016, USA.
Mol Cell. 2004 Nov 19;16(4):505-8. doi: 10.1016/j.molcel.2004.11.008.
The mechanisms underlying somatic hypermutation (SHM) and class switch recombination (CSR) have been the subject of much debate. Recent studies from the Neuberger and Honjo labs have lent insight into these distinct processes, and we discuss a new, comprehensive model for how AID, uracil DNA glycosylase (UNG) and the mismatch repair system function in both SHM and CSR.
体细胞高频突变（SHM）和类别转换重组（CSR）的潜在机制一直是众多争论的焦点。纽伯格实验室和本庶佑实验室最近的研究为这些不同的过程提供了深入见解，并且我们讨论了一个关于活化诱导胞嘧啶脱氨酶（AID）、尿嘧啶DNA糖基化酶（UNG）和错配修复系统如何在SHM和CSR中发挥作用的全新综合模型。
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