Department of Biochemistry and Molecular Genetics (M/C 669), Cancer Center, University of Illinois at Chicago, Chicago, IL, USA.
Cell Cycle. 2009 Dec 15;8(24):4067-71. doi: 10.4161/cc.8.24.10109. Epub 2009 Dec 17.
DDB2 was identified as a protein involved in the Nucleotide Excision Repair (NER), a major DNA repair mechanism that repairs UV damage to prevent accumulation of mutations and tumorigenesis. However, recent studies indicated additional functions of DDB2 in the DNA damage response pathway. Herein, we discuss the proposed mechanisms by which DDB2 activates NER and programmed cell death upon DNA damage through its E3 ligase activity.
DDB2 被鉴定为一种参与核苷酸切除修复(NER)的蛋白质,NER 是一种主要的 DNA 修复机制,可修复 UV 对 DNA 的损伤,防止突变的积累和肿瘤发生。然而,最近的研究表明 DDB2 在 DNA 损伤应答途径中具有额外的功能。本文讨论了 DDB2 通过其 E3 连接酶活性激活 NER 和程序性细胞死亡的可能机制。