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oai:repisalud.isciii.es:20.500.12105/177022024-11-29T16:36:49Zcom_20.500.12105_2173com_20.500.12105_2051col_20.500.12105_19597

00925njm 22002777a 4500 dc Celeste, Arkady author Petersen, Simone author Romanienko, Peter J author Fernandez-Capetillo, Oscar author Chen, Hua Tang author Sedelnikova, Olga A author Reina-San-Martin, Bernardo author Coppola, Vincenzo author Meffre, Eric author Difilippantonio, Michael J author Redon, Christophe author Pilch, Duane R author Olaru, Alexandru author Eckhaus, Michael author Camerini-Otero, R Daniel author Tessarollo, Lino author Livak, Ferenc author Manova, Katia author Bonner, William M author Nussenzweig, Michel C author Nussenzweig, André author 2002-05-03 Higher order chromatin structure presents a barrier to the recognition and repair of DNA damage. Double-strand breaks (DSBs) induce histone H2AX phosphorylation, which is associated with the recruitment of repair factors to damaged DNA. To help clarify the physiological role of H2AX, we targeted H2AX in mice. Although H2AX is not essential for irradiation-induced cell-cycle checkpoints, H2AX-/- mice were radiation sensitive, growth retarded, and immune deficient, and mutant males were infertile. These pleiotropic phenotypes were associated with chromosomal instability, repair defects, and impaired recruitment of Nbs1, 53bp1, and Brca1, but not Rad51, to irradiation-induced foci. Thus, H2AX is critical for facilitating the assembly of specific DNA-repair complexes on damaged DNA. Science . 2002;296(5569):922-7. 10.1126/science.1069398 1095-9203 Science (New York, N.Y.) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4721576/ 11934988 http://hdl.handle.net/20.500.12105/17702 Genomic instability in mice lacking histone H2AX.