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Updated: Jul 15, 2026

Quantification of γH2AX Foci in Response to Ionising Radiation
Published on: April 6, 2010
Genomic instability in mice lacking histone H2AX
Arkady Celeste1, Simone Petersen, Peter J Romanienko
1Experimental Immunology Branch, National Cancer Institute, NIH, Bethesda, MD 20892, USA.
Abstract:
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.
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