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Ctp1 is a cell-cycle-regulated protein that functions with Mre11 complex to control double-strand break repair by homologous recombination.Ctp1是一种细胞周期调控蛋白，它与Mre11复合物共同发挥作用，通过同源重组来控制双链断裂修复。
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DNA双链断裂修复与神经疾病的小鼠模型

Mouse models of DNA double-strand break repair and neurological disease.

作者信息

Frappart Pierre-Olivier, McKinnon Peter J

机构信息

Department Genetics and Tumor Cell Biology, St Jude Children's Research Hospital, Memphis, TN 38105, USA.

出版信息

DNA Repair (Amst). 2008 Jul 1;7(7):1051-60. doi: 10.1016/j.dnarep.2008.03.007. Epub 2008 May 23.

DOI:10.1016/j.dnarep.2008.03.007
PMID:18458002
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3831504/
Abstract

The repair of DNA damage is essential for the prevention of disease. The DNA double-strand break (DSB) is a particularly hazardous lesion. DNA DSBs activate a coordinated cellular response involving cell cycle checkpoint activation and repair of the DNA break, or alternatively apoptosis. In the nervous system the inability to respond to DNA DSBs may lead to neurodegenerative disease or brain tumors. Therefore, understanding the DNA DSB response mechanism in the nervous system is of high importance for developing new treatments for neurodegeneration and cancer. In this regard, the use of mouse models represents an important approach for advancing our understanding of the biology of the DNA damage response in the nervous system.

摘要

DNA损伤的修复对于预防疾病至关重要。DNA双链断裂（DSB）是一种特别危险的损伤。DNA DSB会激活一种协调的细胞反应，包括细胞周期检查点激活和DNA断裂修复，或者诱导细胞凋亡。在神经系统中，无法对DNA DSB做出反应可能会导致神经退行性疾病或脑肿瘤。因此，了解神经系统中的DNA DSB反应机制对于开发神经退行性疾病和癌症的新治疗方法至关重要。在这方面，使用小鼠模型是推进我们对神经系统中DNA损伤反应生物学理解的重要方法。