Human CST abundance determines recovery from diverse forms of DNA damage and replication stress
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Summary
The results suggest that CST is needed in stoichiometric amounts to facilitate re-initiation of DNA replication at repaired forks and/or dormant origins and facilitates recovery from many, but not all, forms of exogenous DNA damage.
- Type
- article
- Published
- 2014-10-29
- Cited by
- 50
- References
- 66
- Access
- Open access
- OpenAlex
- https://openalex.org/W1966392950
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:1542148
Keywords
Aphidicolin, Biology, DNA replication, DNA damage, Cell biology
References
- Structural basis for telomeric single-stranded DNA recognition by yeast Cdc13.
- The Effect of a DNA Repair Gene on Cellular Invasiveness: Xrcc3 Over-Expression in Breast Cancer Cells
- The DNA damage checkpoint response to replication stress: A Game of Forks
- Arrest of replication forks by drug-stabilized topoisomerase I-DNA cleavable complexes as a mechanism of cell killing by camptothecin.
- Human CST promotes telomere duplex replication and general replication restart after fork stalling
- The Saccharomyces telomere-binding protein Cdc13p interacts with both the catalytic subunit of DNA polymerase alpha and the telomerase-associated est1 protein.
- CST meets shelterin to keep telomeres in check.
- RPA-like mammalian Ctc1-Stn1-Ten1 complex binds to single-stranded DNA and protects telomeres independently of the Pot1 pathway.
- Methylated DNA causes a physical block to replication forks independently of damage signalling, O(6)-methylguanine or DNA single-strand breaks and results in DNA damage.
- Evolution of CST function in telomere maintenance
- RTEL1 Is a Replisome-Associated Helicase That Promotes Telomere and Genome-Wide Replication
- Gene expression profiling of the tumor microenvironment during breast cancer progression
- The FANCM/FAAP24 Complex is Required for the DNA Inter-strand Crosslink-Induced Checkpoint Response
- Correlation of microarray-based breast cancer molecular subtypes and clinical outcomes: implications for treatment optimization
- The human CST complex is a terminator of telomerase activity
- Telomeres: Structures in need of unwinding
- Telomere capping proteins are structurally related to RPA with an additional telomere-specific domain
- ATR prohibits replication catastrophe by preventing global exhaustion of RPA.
- Methylating agents and DNA repair responses: Methylated bases and sources of strand breaks.
- Rad51 Expression Is a Useful Predictive Factor for the Efficacy of Neoadjuvant Chemoradiotherapy in Squamous Cell Carcinoma of the Esophagus
Cited by
- Human CST Prefers G-Rich but Not Necessarily Telomeric Sequences
- Emerging roles of CST in maintaining genome stability and human disease
- Structure and function of the telomeric CST complex
- The molecular genetics of the telomere biology disorders
- Suppression of STN1 enhances the cytotoxicity of chemotherapeutic agents in cancer cells by elevating DNA damage
- Human CST facilitates genome-wide RAD51 recruitment to GC-rich repetitive sequences in response to replication stress
- Tying up the Ends: Plasticity in the Recognition of ssDNA at Telomeres
- STN1 OB Fold Mutation Alters DNA Binding and Affects Selective Aspects of CST Function
- Replication stalling and DNA microsatellite instability
- MTV, an ssDNA Protecting Complex Essential for Transposon-Based Telomere Maintenance in Drosophila
- Progress in Human and Tetrahymena Telomerase Structure
- The Role of Telomere Maintenance in Adult Mammalian Acute Central Nervous System Injury and Retinal Ganglion Cell Apoptosis
- Common Chemical Inductors of Replication Stress: Focus on Cell-Based Studies
- CTC1-mediated C-strand fill-in is an essential step in telomere length maintenance
- DNA Replication Origins and Fork Progression at Mammalian Telomeres
- Dynamic DNA binding, junction recognition and G4 melting activity underlie the telomeric and genome-wide roles of human CST
- Pathogenic CTC1 mutations cause global genome instabilities under replication stress
- Mammalian CST averts replication failure by preventing G-quadruplex accumulation
- CTC1-STN1 terminates telomerase while STN1-TEN1 enables C-strand synthesis during telomere replication in colon cancer cells
- Human CST suppresses origin licensing and promotes AND-1/Ctf4 chromatin association
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