摘要
脱氧核糖核酸失配修理(MMR ) 是在维持 genomic 稳定性起一个关键作用的一条高度保存的生物小径。MMR 的特性主要为在 DNA 和再结合期间产生的基础底的失配和插入 / 删除错误对。MMR 也压制 homeologous 再结合并且是最近显示损坏在真核细胞的房间发信号在脱氧核糖核酸起一个作用。分别地， Escherichia 关口 i 傻瓜和 MutL 和他们的真核细胞的相当或相同的事物， MutSalpha 和 MutLalpha 是在联系 MMR 的染色体维护的关键播放器。参予各种各样的脱氧核糖核酸的许多另外的蛋白质部件新陈代谢的小径例如 PCNA 和 RPA，为 MMR 也是必要的。在 MMR 的缺点与染色体宽的不稳定性被联系，倾向到包括世袭 non-polyposis 颜色的癌症的某些类型表面的癌症，到某些化学疗法的代理人的抵抗，和在成熟分裂的畸形和在哺乳动物的系统的绝育。
DNA mismatch repair （MMR） is a highly conserved biological pathway that plays a key role in maintaining genomic stability. The specificity of MMR is primarily for base-base mismatches and insertion/deletion mispairs generated during DNA replication and recombination. MMR also suppresses homeologous recombination and was recently shown to play a role in DNA damage signaling in eukaryotic cells. Escherichia coli MutS and MutL and their eukaryotic homologs, MutSα and MutLα, respectively, are key players in MMR-associated genome maintenance. Many other protein components that participate in various DNA metabolic pathways, such as PCNA and RPA, are also essential for MMR. Defects in MMR are associated with genome-wide instability, predisposition to certain types of cancer including hereditary non-polyposis colorectal cancer, resistance to certain chemotherapeutic agents, and abnormalities in meiosis and sterility in mammalian systems.
