Abstract
DNA repair via homologous recombination (HR) confers cellular resistance to ionizing radiation and certain DNA damaging agents. RAD51 protein momomers assemble into helical filaments at sites of double-stranded DNA breaks; this is a critical event required for the initiation of HR. A central hypothesis of this project is that pharmacologic manipulation of RAD51 may be used to modulate cellular resistance. This represents the final report based on funding from an ASTRO Junior Faculty Research Training Award.
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