Article
Genomic instability in mice lacking histone H2AX.
Science (New York, N.Y.) - 3 May 2002
Celeste Arkady, Petersen Simone, Romanienko Peter J, Fernandez-Capetillo Oscar, Chen Hua Tang, Sedelnikova Olga A, Reina-San-Martin Bernardo, Coppola Vincenzo, Meffre Eric, Difilippantonio Michael J, Redon Christophe, Pilch Duane R, Olaru Alexandru, Eckhaus Michael, Camerini-Otero R Daniel, Tessarollo Lino, Livak Ferenc, Manova Katia, Bonner William M, Nussenzweig Michel C, Nussenzweig André
Abstract excerpt
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...
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