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Int. J. Mol. Sci. 2017, 18(9), 1979;

Genome Instability and γH2AX

Department of Biochemistry & Molecular Biology, Faculty of Biology, University of Athens, Athens 15784, Greece
First Department of Pediatrics “Aghia Sophia” Children’s Hospital, School of Medical, University of Athens, Athens 11527, Greece
EpigenFocus, Athens 11741, Greece
Author to whom correspondence should be addressed.
Received: 21 August 2017 / Revised: 11 September 2017 / Accepted: 12 September 2017 / Published: 15 September 2017
(This article belongs to the Special Issue Mechanisms Leading to Genomic Instability)
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γH2AX has emerged in the last 20 years as a central player in the DDR (DNA damage response), with specificity for DSBs (double-strand breaks). Upon the generation of DSBs, γ-phosphorylation extends along megabase-long domains in chromatin, both sides of the damage. The significance of this mechanism is of great importance; it depicts a biological amplification mechanism where one DSB induces the γ-phosphorylation of thousands of H2AX molecules along megabaselong domains of chromatin, that are adjusted to the sites of DSBs. A sequential recruitment of signal transduction factors that interact to each other and become activated to further amplify the signal that will travel to the cytoplasm take place on the γ-phosphorylated chromatin. γ-phosphorylation is an early event in the DSB damage response, induced in all phases of the cell cycle, and participates in both DSB repair pathways, the HR (homologous recombination) and NHEJ (non-homologous end joining). Today, numerous studies support the notion that γH2AX functions as a guardian of the genome by preventing misrepaired DSB that increase the mutation load of the cells and may further lead to genome instability and carcinogenesis. View Full-Text
Keywords: γH2AX; H2AX; DNA damage; DDR; DSB; DSB repair; epigenetics; epigenetic biomarker γH2AX; H2AX; DNA damage; DDR; DSB; DSB repair; epigenetics; epigenetic biomarker

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Georgoulis, A.; Vorgias, C.E.; Chrousos, G.P.; Rogakou, E.P. Genome Instability and γH2AX. Int. J. Mol. Sci. 2017, 18, 1979.

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