Dysregulation of DNA polymerase κ recruitment to replication forks results in genomic instability
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Summary
It is shown that aberrant recruitment of TLS Polκ to replication forks results in genomic instability and can be mediated through the loss of the deubiquitinase USP1 and proposed a mechanism whereby reversible ubiquitination of PCNA can prevent spurious TLS Pol recruitment and regulate replication fork speed to ensure the maintenance of genome integrity.
- Type
- article
- Published
- 2011-12-13
- Cited by
- 66
- References
- 75
- Access
- Open access
- OpenAlex
- https://openalex.org/W1794195058
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:20408011
Keywords
Biology, Genome instability, Proliferating cell nuclear antigen, DNA replication, Deubiquitinating enzyme
References
- Targeting of human DNA polymerase ι to the replication machinery via interaction with PCNA
- Interaction of human DNA polymerase eta with monoubiquitinated PCNA: a possible mechanism for the polymerase switch in response to DNA damage.
- Regulation of proliferating cell nuclear antigen ubiquitination in mammalian cells
- Chromosomal translocations in yeast induced by low levels of DNA polymerase a model for chromosome fragile sites.
- Replication stress induces sister-chromatid bridging at fragile site loci in mitosis
- The E3 ubiquitin ligase RAD18 regulates ubiquitylation and chromatin loading of FANCD2 and FANCI.
- Participation of mouse DNA polymerase ι in strand-biased mutagenic bypass of UV photoproducts and suppression of skin cancer
- Sequential and Synergistic Modification of Human RPA Stimulates Chromosomal DNA Repair*
- Emergence of Micronuclei and Their Effects on the Fate of Cells under Replication Stress
- Inactivation of Murine Usp1 Results in Genomic Instability and a Fanconi Anemia Phenotype
- Deubiquitination of FANCD2 Is Required for DNA Crosslink Repair
- Regulation of translesion synthesis DNA polymerase eta by monoubiquitination.
- Purification and characterization of pol kappa, a DNA polymerase encoded by the human DINB1 gene.
- Fidelity and Processivity of DNA Synthesis by DNA Polymerase κ, the Product of the Human DINB1 Gene*
- Heterogeneity of eukaryotic replicons, replicon clusters, and replication foci
- Docking of a specialized PIP box onto chromatin-bound PCNA creates a degron for the ubiquitin ligase CRL4Cdt2
- Proliferating cell nuclear antigen-dependent coordination of the biological functions of human DNA polymerase iota.
- The deubiquitinating enzyme USP1 regulates the Fanconi anemia pathway.
- FANCI is a second monoubiquitinated member of the Fanconi anemia pathway
- Upregulation of Error-Prone DNA Polymerases Beta and Kappa Slows Down Fork Progression Without Activating the Replication Checkpoint
Cited by
- The Fanconi Anemia Pathway in Replication Stress and DNA Crosslink Repair
- The roles of DNA polymerase ζ and the Y family DNA polymerases in promoting or preventing genome instability
- Cyclin Kinase-independent role of p21CDKN1A in the promotion of nascent DNA elongation in unstressed cells
- The identification of translesion DNA synthesis regulators: inhibitors in the spotlight
- Different types of interaction between PCNA and PIP boxes contribute to distinct cellular functions of Y-family DNA polymerases
- Catalytic and non‐catalytic roles of DNA polymerase κ in the protection of human cells against genotoxic stresses
- Cheminformatics models based on machine learning approaches for design of USP1/UAF1 abrogators as anticancer agents
- Deubiquitylating Enzymes and DNA Damage Response Pathways
- Characterization of human Spartan/C1orf124, an ubiquitin-PCNA interacting regulator of DNA damage tolerance
- Mismatch repair protein MSH2 regulates translesion DNA synthesis following exposure of cells to UV radiation
- Role of DNA polymerase κ in the maintenance of genomic stability
- Roadworks of DNA Damage Bypass during and after Replication
- The WD40-repeat protein-containing deubiquitinase complex: catalysis, regulation, and potential for therapeutic intervention
- DUB-resistant ubiquitin to survey ubiquitination switches in mammalian cells
- Deubiquitinases as a signaling target of oxidative stress
- N-Aroyl Indole Thiobarbituric Acids as Inhibitors of DNA Repair and Replication Stress Response Polymerases
- The Auto-Generated Fragment of the Usp1 Deubiquitylase Is a Physiological Substrate of the N-End Rule Pathway
- Recombinase and translesion DNA polymerase decrease the speed of replication fork progression during the DNA damage response in Escherichia coli cells
- The deubiquitinating protein USP24 interacts with DDB2 and regulates DDB2 stability
- Regulation of DNA cross-link repair by the Fanconi anemia/BRCA pathway.
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