Structure and positional stability of damaged protein domains in mammalian cells after high LET exposure
نویسندگان
چکیده
Exposure of mammalian cell nuclei with charged particles leads to the spatially defined production of damaged chromatin domains along the particle trajectories. Analysis of track morphology facilitates studies on the dynamics of radiation-induced protein foci associated with lesion processing. Recently we described the discrete formation of γ-H2AX foci and the recruitment of repair related proteins along ion trajectories over a LET range from 200 to 14300 keV/μm in human fibroblasts and in HeLa cells (Fig. 1)[1].
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