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- W2892789620 endingPage "2909" @default.
- W2892789620 startingPage "2909" @default.
- W2892789620 abstract "The complete and accurate replication of the genome is a crucial aspect of cell proliferation that is often perturbed during oncogenesis. Replication stress arising from a variety of obstacles to replication fork progression and processivity is an important contributor to genome destabilization. Accordingly, cells mount a complex response to this stress that allows the stabilization and restart of stalled replication forks and enables the full duplication of the genetic material. This response articulates itself on three important platforms, Replication Protein A/RPA-coated single-stranded DNA, the DNA polymerase processivity clamp PCNA and the FANCD2/I Fanconi Anemia complex. On these platforms, the recruitment, activation and release of a variety of genome maintenance factors is regulated by post-translational modifications including mono- and poly-ubiquitylation. Here, we review recent insights into the control of replication fork stability and restart by the ubiquitin system during replication stress with a particular focus on human cells. We highlight the roles of E3 ubiquitin ligases, ubiquitin readers and deubiquitylases that provide the required flexibility at stalled forks to select the optimal restart pathways and rescue genome stability during stressful conditions." @default.
- W2892789620 created "2018-10-05" @default.
- W2892789620 creator A5026859412 @default.
- W2892789620 creator A5032043749 @default.
- W2892789620 date "2018-09-25" @default.
- W2892789620 modified "2023-10-10" @default.
- W2892789620 title "Ubiquitylation at the Fork: Making and Breaking Chains to Complete DNA Replication" @default.
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