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Endogenous DNA lesions that escape repair will arrest the replication fork, causing replicational stress and genome instability. Mice deficient in the mutagenic translesion synthesis (TLS) protein Rev1 as well as mice with a double deficiency in Rev1 and in Xpc, involved in the repair of such DNA lesions have been generated. The researcher will investigate, in multiple tissues in these mice and in cultured cells, cellular features of ageing, such as proliferation and replication rates, replic...
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