Eva Petermann

Summary

Affiliation: University of Birmingham
Country: UK

Publications

  1. ncbi Chk1 promotes replication fork progression by controlling replication initiation
    Eva Petermann
    Gray Institute for Radiation Oncology and Biology, University of Oxford, Old Road Campus Research Building, Oxford OX3 7DQ, United Kingdom
    Proc Natl Acad Sci U S A 107:16090-5. 2010
  2. ncbi Pathways of mammalian replication fork restart
    Eva Petermann
    University of Birmingham, UK
    Nat Rev Mol Cell Biol 11:683-7. 2010
  3. ncbi Hydroxyurea-stalled replication forks become progressively inactivated and require two different RAD51-mediated pathways for restart and repair
    Eva Petermann
    Gray Institute for Radiation Oncology and Biology, University of Oxford, Oxford OX3 7DQ, UK
    Mol Cell 37:492-502. 2010
  4. ncbi Replication fork dynamics and the DNA damage response
    Rebecca M Jones
    School of Cancer Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK
    Biochem J 443:13-26. 2012
  5. ncbi DNA repair pathways as targets for cancer therapy
    Thomas 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

Collaborators

Detail Information

Publications5

  1. ncbi Chk1 promotes replication fork progression by controlling replication initiation
    Eva Petermann
    Gray Institute for Radiation Oncology and Biology, University of Oxford, Old Road Campus Research Building, Oxford OX3 7DQ, United Kingdom
    Proc Natl Acad Sci U S A 107:16090-5. 2010
    ..Our data suggest that increased replication initiation leads to slow replication fork progression and that Chk1 promotes replication fork progression during normal S phase by controlling replication origin activity...
  2. ncbi Pathways of mammalian replication fork restart
    Eva Petermann
    University of Birmingham, UK
    Nat Rev Mol Cell Biol 11:683-7. 2010
    ..Different models of replication fork restart can be envisaged, based on the involvement of DNA helicases, nucleases, homologous recombination factors and the importance of DNA double-strand break formation...
  3. ncbi Hydroxyurea-stalled replication forks become progressively inactivated and require two different RAD51-mediated pathways for restart and repair
    Eva Petermann
    Gray Institute for Radiation Oncology and Biology, University of Oxford, Oxford OX3 7DQ, UK
    Mol Cell 37:492-502. 2010
    ..In conclusion, our data suggest that restart of stalled replication forks and HR repair of collapsed replication forks require two distinct RAD51-mediated pathways...
  4. ncbi Replication fork dynamics and the DNA damage response
    Rebecca M Jones
    School of Cancer Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK
    Biochem J 443:13-26. 2012
    ..If replication fork progression fails to be rescued, this may lead to DNA damage and genomic instability via nuclease processing of aberrant fork structures or incomplete sister chromatid separation during mitosis...
  5. ncbi DNA repair pathways as targets for cancer therapy
    Thomas 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
    ....