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Regulation of Histone Ubiquitination in Response to DNA Double Strand Breaks
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The Chromatin Response to Double-Strand DNA Breaks and Their Repair

Roumen Tsanev Institute of Molecular Biology, Bulgarian Academy of Sciences, Acad. G. Bonchev Str. 21, 1113 Sofia, Bulgaria
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Cells 2020, 9(8), 1853; https://doi.org/10.3390/cells9081853
Received: 15 June 2020 / Revised: 3 August 2020 / Accepted: 4 August 2020 / Published: 7 August 2020
(This article belongs to the Special Issue Double-Strand DNA Break Repair and Human Disease)
Cellular DNA is constantly being damaged by numerous internal and external mutagenic factors. Probably the most severe type of insults DNA could suffer are the double-strand DNA breaks (DSBs). They sever both DNA strands and compromise genomic stability, causing deleterious chromosomal aberrations that are implicated in numerous maladies, including cancer. Not surprisingly, cells have evolved several DSB repair pathways encompassing hundreds of different DNA repair proteins to cope with this challenge. In eukaryotic cells, DSB repair is fulfilled in the immensely complex environment of the chromatin. The chromatin is not just a passive background that accommodates the multitude of DNA repair proteins, but it is a highly dynamic and active participant in the repair process. Chromatin alterations, such as changing patterns of histone modifications shaped by numerous histone-modifying enzymes and chromatin remodeling, are pivotal for proficient DSB repair. Dynamic chromatin changes ensure accessibility to the damaged region, recruit DNA repair proteins, and regulate their association and activity, contributing to DSB repair pathway choice and coordination. Given the paramount importance of DSB repair in tumorigenesis and cancer progression, DSB repair has turned into an attractive target for the development of novel anticancer therapies, some of which have already entered the clinic. View Full-Text
Keywords: DNA damage response; double-strand DNA break repair; non-homologous end joining; homologous recombination; chromatin dynamics in DNA repair; synthetic lethality; PARP inhibitors; cancer; anticancer drug therapies DNA damage response; double-strand DNA break repair; non-homologous end joining; homologous recombination; chromatin dynamics in DNA repair; synthetic lethality; PARP inhibitors; cancer; anticancer drug therapies
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MDPI and ACS Style

Aleksandrov, R.; Hristova, R.; Stoynov, S.; Gospodinov, A. The Chromatin Response to Double-Strand DNA Breaks and Their Repair. Cells 2020, 9, 1853. https://doi.org/10.3390/cells9081853

AMA Style

Aleksandrov R, Hristova R, Stoynov S, Gospodinov A. The Chromatin Response to Double-Strand DNA Breaks and Their Repair. Cells. 2020; 9(8):1853. https://doi.org/10.3390/cells9081853

Chicago/Turabian Style

Aleksandrov, Radoslav, Rossitsa Hristova, Stoyno Stoynov, and Anastas Gospodinov. 2020. "The Chromatin Response to Double-Strand DNA Breaks and Their Repair" Cells 9, no. 8: 1853. https://doi.org/10.3390/cells9081853

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