Notably, human XKD fetal brain neurons showed a trend, though not statistically significant, towards increased DNA damage in the untreated samples relative to the controls (see Figure 6 B), suggesting that there could exist a set of ataxia patients that arise from genetic defects in XRCC1 .
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XRCC1 protects against the lethality of induced oxidative DNA damage in nondividing neural cells.
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