Abstract
The two major double-strand break (DSB) repair pathways, homologous recombination (HR), and non-homologous end joining (NHEJ) play a critical role in the response to ionizing radiation (IR). Furthermore, it is well established that disrupting the balance between NHEJ and HR induces significant radiosensitivity. The rare cutting restriction endonuclease, I-SceI, is utilized commonly to assess intrachromosomal DSB repair in mammalian cells. We sought to develop an I-SceI-based assay and high-throughput screening platform to screen for drugs which modulate DSB repair.
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