Affiliation: University of Sussex
- Chk1 requirement for high global rates of replication fork progression during normal vertebrate S phaseEva Petermann
Genome Damage and Stability Centre, University of Sussex, Science Park Road, Falmer, Brighton BN1 9RQ, UK
Mol Cell Biol 26:3319-26. 2006....
- Evidence that the ATR/Chk1 pathway maintains normal replication fork progression during unperturbed S phaseEva Petermann
Genome Damage and Stability Centre, University of Sussex, Falmer, Brighton, UK
Cell Cycle 5:2203-9. 2006..Here we give an overview of how the ATR/Chk1 pathway responds to exogenously blocked replication and then describe evidence for roles of this pathway during replication in an unperturbed S phase...
- Claspin promotes normal replication fork rates in human cellsEva Petermann
Genome Damage and Stability Centre, University of Sussex, Falmer, Brighton BN1 9RQ, United Kingdom
Mol Biol Cell 19:2373-8. 2008..Consistent with this possibility, depletion of Chk1 and Claspin together doubled the percentage of very slow forks, compared with depletion of either protein alone...
- ATR-dependent phosphorylation and activation of ATM in response to UV treatment or replication fork stallingThomas Stiff
Genome Damage and Stability Centre, University of Sussex, Falmer, Brighton, East Sussex, UK
EMBO J 25:5775-82. 2006..Our findings provide insight into the interplay between the PIKK damage response pathways...
- Diminished origin-licensing capacity specifically sensitizes tumor cells to replication stressKristin M Zimmerman
University of Sussex, Falmer, Brighton BN1 9RQ, United Kingdom
Mol Cancer Res 11:370-80. 2013..Collectively, these findings suggest that tumor cells may have a reliance on origin-licensing capacity, suggesting that licensing factors could represent a target for drug-based cancer therapy...
- Measurement of chromosomal DNA single-strand breaks and replication fork progression ratesClaire Breslin
Genome Damage and Stability Center, University of Sussex, Brighton, United Kingdom
Methods Enzymol 409:410-25. 2006..We also describe an assay we employ to measure the rate of replication fork progression in mammalian/vertebrate cells in the presence or absence of DNA damage...
- Chk1 regulates the density of active replication origins during the vertebrate S phaseApolinar Maya-Mendoza
Faculty of Life Sciences, University of Manchester, MIB, Manchester, UK
EMBO J 26:2719-31. 2007..The same phenotype is induced in wild-type avian cells when Chk1 or ATM/ATR is inhibited. These observations show that Chk1 regulates replication origin activation and contributes to S-phase progression in somatic vertebrate cells...
- DNA repair pathways as targets for cancer therapyThomas Helleday
Radiation Oncology and Biology, University of Oxford, Old Road Campus Research Building, off Roosevelt Drive, Headington, Oxford, OX3 7DQ, UK
Nat Rev Cancer 8:193-204. 2008....
- Roles of DNA ligase III and XRCC1 in regulating the switch between short patch and long patch BEREva Petermann
Institut fur Biochemie, Freie Universitat Berlin, Thielallee 63, 14195 Berlin, Federal Republic of Germany
DNA Repair (Amst) 5:544-55. 2006..Accordingly, lowering the levels of the XRCC1/Lig III complex in HeLa cells using siRNA decreases ligation capacity but enhances Pol beta-dependent DNA synthesis...
- ATP-dependent selection between single nucleotide and long patch base excision repairEva Petermann
Institut fur Biochemie, Freie Universitat Berlin, Thielallee 63, 14195, Berlin, Germany
DNA Repair (Amst) 2:1101-14. 2003..It is proposed that long patch BER is required for ATP generation from poly(ADP-ribose) and, therefore, predominant under conditions of ATP shortage...