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The ubiquitin‐ and SUMO‐dependent signaling response to DNA double‐strand breaks
Author(s) -
Bekker-Jensen Simon,
Mailand Niels
Publication year - 2011
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2011.05.056
Subject(s) - ubiquitin , double strand , chemistry , dna , microbiology and biotechnology , dna damage , biophysics , biochemistry , biology , gene
DNA double‐strand breaks (DSBs) represent the most destructive type of chromosomal lesion and trigger rapid chromatin restructuring accompanied by accumulation of proteins in the vicinity of the DSB. Non‐proteolytic ubiquitylation of chromatin surrounding DSBs, mediated by the RNF8/RNF168 ubiquitin ligase cascade, has emerged as a key mechanism for restoration of genome integrity by licensing the DSB‐modified chromatin to concentrate genome caretaker proteins such as 53BP1 and BRCA1 near the lesions. In parallel, SUMOylation of upstream DSB regulators is also required for execution of this ubiquitin‐dependent chromatin response, but its molecular basis is currently unclear. Here, we discuss recent insights into how ubiquitin‐ and SUMO‐dependent signaling processes cooperate to orchestrate protein interactions with sites of DNA damage to facilitate DSB repair.