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- W2478163165 abstract "This chapter discusses the checkpoint kinase and Wee1 inhibitors as anticancer therapeutics. DNA damage triggers recruitment of multi-protein complexes (sensors) that then activate the transducers ATM (ataxia telangiectesia mutated) and ATR (ATM and Rad3 related). It is generally accepted that ATR activation is driven by single-strand breaks (SSBs) formed as a result of stalled replication forks, whereas ATM is the main initiator of response to double-strand breaks (DSBs) resulting from ionizing radiation and other types of DNA damage. These mechanisms (collectively termed the DNA-damage response [DDR]) detect DNA lesions, signal their presence and promote their repair by the initiation of cell cycle arrest, repair processes, or apoptotic responses. The DDR is now recognized to be a comprehensive and complex set of responses aimed at safeguarding the genomic integrity of cells. DNA repair processes lay the foundation of this response with additional networks of monitoring leading to the activation of cell cycle checkpoints or apoptosis." @default.
- W2478163165 created "2016-08-23" @default.
- W2478163165 creator A5053711252 @default.
- W2478163165 date "2012-01-01" @default.
- W2478163165 modified "2023-10-16" @default.
- W2478163165 title "Checkpoint Kinase and Wee1 Inhibitors as Anticancer Therapeutics" @default.
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