Oncogenes induce genotoxic stress by mitotic processing of unusual replication intermediates
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Summary
Processing of unusual replication intermediates such as reversed forks by MUS81 contributes to oncogene-induced double-strand breaks and depends on mitotic entry.
- Type
- article
- Published
- 2013-03-18
- Cited by
- 199
- References
- 50
- Access
- Open access
- OpenAlex
- https://openalex.org/W23479741
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:11343579
Keywords
Art
References
- Visualization and interpretation of eukaryotic DNA replication intermediates in vivo by electron microscopy.
- DNA damage signalling guards against activated oncogenes and tumour progression
- Increased replication initiation and conflicts with transcription underlie Cyclin E-induced replication stress
- The structure‐specific endonuclease Mus81–Eme1 promotes conversion of interstrand DNA crosslinks into double‐strands breaks
- The Replication Checkpoint Protects Fork Stability by Releasing Transcribed Genes from Nuclear Pores
- A model for replication repair in mammalian cells.
- Topoisomerase I poisoning results in PARP-mediated replication fork reversal
- Structure-Specific DNA Endonuclease Mus81/Eme1 Generates DNA Damage Caused by Chk1 Inactivation
- Preventing replication stress to maintain genome stability: resolving conflicts between replication and transcription.
- Persistent telomere damage induces by-pass of mitosis and tetraploidy
- 53BP1 nuclear bodies form around DNA lesions generated by mitotic transmission of chromosomes under replication stress
- The WRN and MUS81 proteins limit cell death and genome instability following oncogene activation
- Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints
- The structure-specific endonuclease Mus81 contributes to replication restart by generating double-strand DNA breaks
- Fork Reversal and ssDNA Accumulation at Stalled Replication Forks Owing to Checkpoint Defects
- DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis
- Monoclonal antibodies to mitotic cells.
- A cell-based screen identifies ATR inhibitors with synthetic lethal properties for cancer-associated mutations
- Non-transcriptional control of DNA replication by c-Myc
- Replicon Clusters Are Stable Units of Chromosome Structure: Evidence That Nuclear Organization Contributes to the Efficient Activation and Propagation of S Phase in Human Cells
Cited by
- HEK293 in cell biology and cancer research: phenotype, karyotype, tumorigenicity, and stress-induced genome-phenotype evolution.
- Visualization and interpretation of eukaryotic DNA replication intermediates in vivo by electron microscopy.
- Cancer therapy and replication stress: forks on the road to perdition.
- Interactions between mitochondria and inflammatory factors during cellular senescence
- Cyclin E Deregulation Promotes Loss of Specific Genomic Regions
- Replication Stress in Mammalian Cells and Its Consequences for Mitosis
- The Mismatch-Binding Factor MutSβ Can Mediate ATR Activation in Response to DNA Double-Strand Breaks.
- Mammalian RAD51 paralogs protect nascent DNA at stalled forks and mediate replication restart
- Distinct but Concerted Roles of ATR, DNA-PK, and Chk1 in Countering Replication Stress during S Phase
- HLTF’s Ancient HIRAN Domain Binds 3′-DNA Ends to Drive Replication Fork Reversal
- Theoretical considerations for thresholds in chemical carcinogenesis.
- ATR and a Chk1-Aurora B pathway coordinate postmitotic genome surveillance with cytokinetic abscission
- DNA replication and oncogene-induced replicative stress.
- The DNA repair endonuclease Mus81 facilitates fast DNA replication in the absence of exogenous damage
- Oncogenes induce a reversal of replication’s fortunes
- Replication fork reversal in eukaryotes: from dead end to dynamic response
- Metabolism of DNA secondary structures at the eukaryotic replication fork.
- Replication forks reverse at high frequency upon replication stress in Physarum polycephalum
- The DNA damage response during mitosis.
- Molecular Mechanisms of DNA Replication Checkpoint Activation
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