Friday, July 23, 2010, 11:00 am — John Dunn Seminar Room, Bldg. 463
The choice of the particular DNA repair pathway(s) that irradiated mammalian cells employ to mediate the repair of various ionizing radiation (IR)-induced DNA lesions and assure the continued genomic integrity of surviving cells depends strongly on the position of exposed cells within their division cycle. Of particular importance concerning risks for IR-induced carcinogenesis is the complex interplay between the two primary DNA double-strand break (DSB) repair pathways, non-homologous end-joining (NHEJ) and homologous recombinational repair (HRR), as their activities can dramatically impact the induction of carcinogenic chromosomal aberrations and mutations in irradiated cells undergoing DNA replication. I will discuss recent and ongoing studies from my laboratory that further define the roles of these essential DSB repair pathways during the different cell cycle phases in primary human fibroblasts and gene-targeted Chinese hamster ovary (CHO) cells deficient in key DSB signaling and repair proteins following exposure to low to moderates doses of IR.
Hosted by: Paul Freimuth
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