期刊
OPEN BIOLOGY
卷 5, 期 4, 页码 -出版社
ROYAL SOC
DOI: 10.1098/rsob.150018
关键词
DNA damage response; double-strand break repair; ubiquitin; NEDD8; MLN4924
资金
- Wellcome Trust Clinical Fellowship [094794/Z/10/Z]
- Cancer Research UK [C6/A11224]
- European Research Council
- European Community [HEALTH-F2-2010-259893]
- CRUK [C6946/A14492]
- Wellcome Trust [WT092096]
- University of Cambridge UK
- Wellcome Trust [094794/Z/10/Z] Funding Source: Wellcome Trust
- Cancer Research UK [11224, 18796] Funding Source: researchfish
Failure of accurate DNA damage sensing and repair mechanisms manifests as a variety of human diseases, including neurodegenerative disorders, immunodeficiency, infertility and cancer. The accuracy and efficiency of DNA damage detection and repair, collectively termed the DNA damage response (DDR), requires the recruitment and subsequent post-translational modification (PTM) of a complex network of proteins. Ubiquitin and the ubiquitin-like protein (UBL) SUMO have established roles in regulating the cellular response to DNA double-strand breaks (DSBs). A role for other UBLs, such as NEDD8, is also now emerging. This article provides an overview of the DDR, discusses our current understanding of the process and function of PTM by ubiquitin and NEDD8, and reviews the literature surrounding the role of ubiquitylation and neddylation in DNA repair processes, focusing particularly on DNA DSB repair.
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