AI Article Synopsis
- Failure of proper DNA damage sensing and repair can lead to serious diseases, including neurodegenerative disorders, cancer, and infertility.
- The DNA damage response (DDR) relies on a network of proteins activated through post-translational modifications (PTMs), particularly by molecules like ubiquitin and SUMO.
- The article reviews current research on the DDR, emphasizing the roles of ubiquitylation and neddylation in repairing DNA double-strand breaks (DSBs).
Article Abstract
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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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4422126 | PMC |
| http://dx.doi.org/10.1098/rsob.150018 | DOI Listing |
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