생화학분자생물학회입니다.
DNA end resection and its role in DNA replication and DSB repair choice in mammalian cells
작성자
관리자작성일자
2020-12-23조회수
119Zhenkun Lou ( Lou.zhenkun@mayo.edu ) | ||
2013-present | Professor, Department of Pharmacology, Mayo Clinic | |
2012-present | Consultant, Division of Oncology Research, Department of Oncology, Mayo Clinic. | |
2011-present | Co-Chair, Developmental Therapeutics Program, Mayo Clinic Cancer Center | |
2009-2012 | Associate Professor, Department of Pharmacology, Mayo Clinic | |
2009-2012 | Senior Associate Consultant, Division of Oncology Research, Department of Oncology, Mayo Clinic | |
2006-2009 | Assistant Professor and Associate Consultant, Division of Oncology Research, Department of Oncology, Mayo Clinic | |
2001-2006 | Postdoctoral Research Fellow, Department of Oncology, Mayo Medical Center | |
1992-1995 | Research Fellow, Shanghai Research Center for Biotechnology, Academia SINICA, Shanghai, China. |
DNA end resection and its role in DNA replication and DSB repair choice in mammalian cells
DNA end resection has a key role in double-strand break repair and DNA replication. Defective DNA end resection can cause malfunctions in DNA repair and replication, leading to greater genomic instability. DNA end resection is initiated by MRN-CtIP generating short, 3'-single-stranded DNA (ssDNA). This newly generated ssDNA is further elongated by multiple nucleases and DNA helicases, such as EXO1, DNA2, and BLM. Effective DNA end resection is essential for error-free homologous recombination DNA repair, the degradation of incorrectly replicated DNA and double-strand break repair choice. Because of its importance in DNA repair, DNA end resection is strictly regulated. Numerous mechanisms have been reported to regulate the initiation, extension, and termination of DNA end resection. Here, we review the general process of DNA end resection and its role in DNA replication and repair pathway choice..
Exp Mol Med. 2020 Oct;52(10):1705-1714. doi: 10.1038/s12276-020-00519-1.
https://pubmed.ncbi.nlm.nih.gov/33122806/