Targeting ATR for selective cancer therapy
The DNA damage response (DDR), comprising repair and cell cycle checkpoints, maintains genomic stability. DDR dysfunction, particularly loss of the G1 checkpoint (e.g. p53 mutation), is common in cancer increasing reliance on S/G2 checkpoints. ATR, a kinase activated by ssDNA-dsDNA junctions arising...
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University of Newcastle upon Tyne
2014
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| Online Access: | https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.743391 |