The Effects of Chemotherapy Versus Radiation Therapy on Behavior and Neuronal Architecture in the Hippocampus Ca1 Region

methylation, destabilizes RAD52, and reduces focus formation and diffusion rate changes in response to HU. Finally, RAD52-K116R overexpression has a dominant negative effect on cell survival after HU but not IR. Conclusions: Previously, we found that replication stress induces RAD52 co-localization with RAD51, and RAD52 has reduced diffusion consistent with enhanced oligomerization and association with chromatin. This suggests that RAD52 has a role in the response to replication fork arrest. Our results indicate that RAD52 lysine-116 contributes to RAD52 methylation, which regulates RAD52 stability and function in response to replication stress. Since RAD52 is synthetically lethal with BRCA2, this modification may present a novel druggable target to destabilize RAD52 in BRCA2-deficient cancers, conferring synthetic lethality and therapeutic gain similar to that observed with PARP inhibitors. Author Disclosure: J.W. Wray: None. J. Liu: None. M. Shaheen: None. R. Hromas: None. J.A. Nickoloff: None. Z. Shen: None.