More than just a focus: The chromatin response to DNA damage and its role in genome integrity maintenance

By J. Lukas, C. Lukas, J. Bartek. Nature Cell Biology, 2011

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DNA damage and its links to neurodegeneration (2014, positive): “The recruitment of MDC1 coordinates virtually every aspect of the DSB signaling response (Lukas et al., 2011).”
A Liquid-to-Solid Phase Transition of the ALS Protein FUS Accelerated by Disease Mutation. (2015, positive): “Indeed, FUS moves to sites of DNA damage within seconds of a triggering event, presumably forming a compartment that recruits myriad additional factors required for DNA damage repair (Dutertre et al., 2014; Lukas et al., 2011).”
Playing the end game: DNA double-strand break repair pathway choice. (2012, background): “53BP1 enrichment may be regulated by changes in the presentation of the constitutive H4K20me2 epitope at DSB sites, and/or de novo methylation events mediated by lysine methyl-transferases (KMTs) such as PRSET8 or MMSET (reviewed in Lukas et al., 2011).”
DNA damage sensing by the ATM and ATR kinases. (2013, background): “…of numerous DNA repair proteins and chromatin-remodeling complexes around DSBs. Cumulative evidence suggests that ATM is part of the chromatin-mediated program at DSBs that promotes DSB repair and coordinates multiple cellular processes in the chromatin domains flanking DSBs (Lukas et al. 2011).”
53BP1 is a reader of the DNA damage-induced H2A Lys15 ubiquitin mark (2013, neutral): “Class switching to IgG1 was assayed in 53BP1 murine primary B cells complemented with 53BP1 (1-1711) and mutants thereof by retroviral delivery.”