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More modifiers move on DNA damage Morris JRCancer Res 2010[May]; 70 (10): 3861-3In mammalian cells the accumulation of repair proteins to double-strand breaks is a phosphorylation- and ubiquitylation-regulated process. Some of the genes that encode the kinases and ubiquitin ligases in this pathway are cancer predisposition genes, most prominently the breast cancer predisposition gene BRCA1, which encodes a ubiquitin ligase. How BRCA1 ligase activity was regulated following DNA damage was poorly understood. In this review I summarize new data that show a third post-translational modification, by the small ubiquitin like modifier SUMO, is part of the same cascade, enabling and activating DNA damage-regulated processes, including the BRCA1 ligase activity.|*DNA Damage[MESH]|*Protein Processing, Post-Translational[MESH]|Animals[MESH]|BRCA1 Protein/*metabolism[MESH]|Humans[MESH]|Small Ubiquitin-Related Modifier Proteins/*metabolism[MESH]|Ubiquitination[MESH] |
