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- W3202216963 endingPage "181" @default.
- W3202216963 startingPage "169" @default.
- W3202216963 abstract "Cells activate distinctive regulatory pathways that prevent excessive initiation of DNA replication to achieve timely and accurate genome duplication. Excess DNA synthesis is constrained by protein-DNA interactions that inhibit initiation at dormant origins. In parallel, specific modifications of pre-replication complexes prohibit post-replicative origin relicensing. Replication stress ensues when the controls that prevent excess replication are missing in cancer cells, which often harbor extrachromosomal DNA that can be further amplified by recombination-mediated processes to generate chromosomal translocations. The genomic instability that accompanies excess replication origin activation can provide a promising target for therapeutic intervention. Here we review molecular pathways that modulate replication origin dormancy, prevent excess origin activation, and detect, encapsulate, and eliminate persistent excess DNA." @default.
- W3202216963 created "2021-10-11" @default.
- W3202216963 creator A5009198169 @default.
- W3202216963 creator A5015342151 @default.
- W3202216963 creator A5044439179 @default.
- W3202216963 creator A5045977241 @default.
- W3202216963 date "2022-02-01" @default.
- W3202216963 modified "2023-09-25" @default.
- W3202216963 title "Preventing excess replication origin activation to ensure genome stability" @default.
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