Dana Branzei

Summary

Affiliation: European Institute of Oncology
Country: Italy

Publications

  1. ncbi Regulation of DNA repair throughout the cell cycle
    Dana Branzei
    FIRC Institute of Molecular Oncology Foundation, Via Adamello 16, 20139 Milan, Italy
    Nat Rev Mol Cell Biol 9:297-308. 2008
  2. ncbi Leaping forks at inverted repeats
    Dana Branzei
    Fondazione IFOM, Istituto FIRC di Oncologia Molecolare, 20139 Milan, Italy
    Genes Dev 24:5-9. 2010
  3. ncbi Template switching: from replication fork repair to genome rearrangements
    Dana Branzei
    FIRC Institute of Molecular Oncology Foundation, Via Adamello 16, 20139 Milan, Italy Universitá degli Studi di Milano, Via Celoria 26, 20133 Milan, Italy
    Cell 131:1228-30. 2007
  4. ncbi Maintaining genome stability at the replication fork
    Dana Branzei
    Fondazione IFOM, Istituto FIRC di Oncologia Molecolare, IFOM IEO Campus, Via Adamello 16, 20139 Milan, Italy
    Nat Rev Mol Cell Biol 11:208-19. 2010
  5. ncbi Interplay of replication checkpoints and repair proteins at stalled replication forks
    Dana Branzei
    FIRC Institute of Molecular Oncology Foundation, Via Adamello 16, 20139 Milan, Italy
    DNA Repair (Amst) 6:994-1003. 2007
  6. ncbi Ubc9- and mms21-mediated sumoylation counteracts recombinogenic events at damaged replication forks
    Dana Branzei
    FIRC Institute of Molecular Oncology Foundation and Department of Biomedical Sciences and Biotechnology, Universita degli Studi di Milano, Via Adamello 16, 20139 Milan, Italy
    Cell 127:509-22. 2006
  7. ncbi SUMOylation regulates Rad18-mediated template switch
    Dana Branzei
    IFOM, the FIRC Institute for Molecular Oncology Foundation, IFOM IEO Campus, Via Adamello 16, 20139 Milan, Italy
    Nature 456:915-20. 2008
  8. ncbi Ubiquitin family modifications and template switching
    Dana Branzei
    Fondazione IFOM, Istituto FIRC di Oncologia Molecolare, IFOM IEO Campus, Via Adamello 16, 20139 Milan, Italy
    FEBS Lett 585:2810-7. 2011
  9. ncbi The checkpoint response to replication stress
    Dana Branzei
    FIRC Institute of Molecular Oncology Foundation IFOM IEO campus, Via Adamello 16, 20139 Milan, Italy
    DNA Repair (Amst) 8:1038-46. 2009
  10. ncbi The Saccharomyces cerevisiae Esc2 and Smc5-6 proteins promote sister chromatid junction-mediated intra-S repair
    Julie Sollier
    IFOM, the FIRC Institute for Molecular Oncology Foundation, IFOM IEO Campus, 20139 Milan, Italy
    Mol Biol Cell 20:1671-82. 2009

Collaborators

Detail Information

Publications22

  1. ncbi Regulation of DNA repair throughout the cell cycle
    Dana Branzei
    FIRC Institute of Molecular Oncology Foundation, Via Adamello 16, 20139 Milan, Italy
    Nat Rev Mol Cell Biol 9:297-308. 2008
    ..Recent studies have provided insights into the mechanisms that contribute to DNA repair in specific cell-cycle phases and have highlighted the mechanisms that ensure cell-cycle progression or arrest in normal and cancerous cells...
  2. ncbi Leaping forks at inverted repeats
    Dana Branzei
    Fondazione IFOM, Istituto FIRC di Oncologia Molecolare, 20139 Milan, Italy
    Genes Dev 24:5-9. 2010
    ..The recombination mechanism underlying this phenomenon does not appear to require double-strand break formation, and is likely caused by a replication mechanism involving template switching...
  3. ncbi Template switching: from replication fork repair to genome rearrangements
    Dana Branzei
    FIRC Institute of Molecular Oncology Foundation, Via Adamello 16, 20139 Milan, Italy Universitá degli Studi di Milano, Via Celoria 26, 20133 Milan, Italy
    Cell 131:1228-30. 2007
    ..2007) show that the complex nonrecurrent rearrangements observed in the dysmyelinating disorder Pelizaeus-Merzbacher disease (PMD) are likely to be caused by a replication mechanism involving template switching...
  4. ncbi Maintaining genome stability at the replication fork
    Dana Branzei
    Fondazione IFOM, Istituto FIRC di Oncologia Molecolare, IFOM IEO Campus, Via Adamello 16, 20139 Milan, Italy
    Nat Rev Mol Cell Biol 11:208-19. 2010
    ..The mechanisms that operate in eukaryotic cells to promote replication fork integrity and coordinate replication with other aspects of chromosome maintenance are becoming clear...
  5. ncbi Interplay of replication checkpoints and repair proteins at stalled replication forks
    Dana Branzei
    FIRC Institute of Molecular Oncology Foundation, Via Adamello 16, 20139 Milan, Italy
    DNA Repair (Amst) 6:994-1003. 2007
    ....
  6. ncbi Ubc9- and mms21-mediated sumoylation counteracts recombinogenic events at damaged replication forks
    Dana Branzei
    FIRC Institute of Molecular Oncology Foundation and Department of Biomedical Sciences and Biotechnology, Universita degli Studi di Milano, Via Adamello 16, 20139 Milan, Italy
    Cell 127:509-22. 2006
    ..Our results indicate that Ubc9- and Mms21-mediated sumoylation functions as a regulatory mechanism, different from that of replication checkpoints, to prevent pathological accumulation of cruciform structures at damaged forks...
  7. ncbi SUMOylation regulates Rad18-mediated template switch
    Dana Branzei
    IFOM, the FIRC Institute for Molecular Oncology Foundation, IFOM IEO Campus, Via Adamello 16, 20139 Milan, Italy
    Nature 456:915-20. 2008
    ..Altogether, our results unmask a role for PCNA ubiquitylation and SUMOylation pathways in promoting transient damage-induced replication-coupled recombination events involving sister chromatids at replication forks...
  8. ncbi Ubiquitin family modifications and template switching
    Dana Branzei
    Fondazione IFOM, Istituto FIRC di Oncologia Molecolare, IFOM IEO Campus, Via Adamello 16, 20139 Milan, Italy
    FEBS Lett 585:2810-7. 2011
    ..Here I review the biological significance of template switching at the nexus of DNA replication and recombination, and the role of ubiquitin-like modifications in mediating and controlling this process...
  9. ncbi The checkpoint response to replication stress
    Dana Branzei
    FIRC Institute of Molecular Oncology Foundation IFOM IEO campus, Via Adamello 16, 20139 Milan, Italy
    DNA Repair (Amst) 8:1038-46. 2009
    ....
  10. ncbi The Saccharomyces cerevisiae Esc2 and Smc5-6 proteins promote sister chromatid junction-mediated intra-S repair
    Julie Sollier
    IFOM, the FIRC Institute for Molecular Oncology Foundation, IFOM IEO Campus, 20139 Milan, Italy
    Mol Biol Cell 20:1671-82. 2009
    ....
  11. ncbi The Rad53 signal transduction pathway: Replication fork stabilization, DNA repair, and adaptation
    Dana Branzei
    FIRC Institute of Molecular Oncology Foundation, Milan, Italy
    Exp Cell Res 312:2654-9. 2006
    ....
  12. ncbi RecQ helicases queuing with Srs2 to disrupt Rad51 filaments and suppress recombination
    Dana Branzei
    Fondazione Italiana Ricerca sul Cancro, Institute of Molecular Oncology Foundation, 20139 Milan, Italy
    Genes Dev 21:3019-26. 2007
  13. ncbi Replication and recombination factors contributing to recombination-dependent bypass of DNA lesions by template switch
    Fabio Vanoli
    Fondazione IFOM, Istituto FIRC di Oncologia Molecolare, Milan, Italy
    PLoS Genet 6:e1001205. 2010
    ..Our results allow us to propose the choreography through which different players contribute to template switch in response to DNA damage and to distinguish this process from other recombination-mediated processes promoting DNA repair...
  14. ncbi The SUMO protease SENP1 is required for cohesion maintenance and mitotic arrest following spindle poison treatment
    Saho Era
    Fondazione IFOM, Istituto FIRC di Oncologia Molecolare, IFOM IEO Campus, Via Adamello 16, 20139 Milan, Italy
    Biochem Biophys Res Commun 426:310-6. 2012
    ..In conclusion, we identify SENP1 as a novel factor required for mitotic arrest and cohesion maintenance during prolonged mitotic arrest induced by spindle poisons...
  15. ncbi Cohesion by topology: sister chromatids interlocked by DNA
    Rodrigo Bermejo
    Fondazione Italiana per la Ricerca sul Cancro FIRC Institute of Molecular Oncology Foundation, 20139 Milan, Italy
    Genes Dev 22:2297-301. 2008
    ..They propose that DNA precatenanes, arising during replication fork progression, hold sister chromatids together...
  16. ncbi The DNA damage response during DNA replication
    Dana Branzei
    FIRC Institute of Molecular Oncology Foundation and DSBB-University of Milan, Via Adamello 16, 20139, Milan, Italy
    Curr Opin Cell Biol 17:568-75. 2005
    ....
  17. ncbi Premature Cdk1/Cdc5/Mus81 pathway activation induces aberrant replication and deleterious crossover
    Barnabas Szakal
    Department of Molecular Oncology, Fondazione IFOM, Istituto FIRC di Oncologia Molecolare, Milan, Italy
    EMBO J 32:1155-67. 2013
    ....
  18. ncbi Rad52 sumoylation and its involvement in the efficient induction of homologous recombination
    Takashi Ohuchi
    Molecular Cell Biology Laboratory, Graduate School of Pharmaceutical Sciences, Tohoku University, Aoba 6 3, Aramaki, Aoba ku, Sendai 980 8578, Japan
    DNA Repair (Amst) 7:879-89. 2008
    ....
  19. ncbi Mgs1 and Rad18/Rad5/Mms2 are required for survival of Saccharomyces cerevisiae mutants with novel temperature/cold sensitive alleles of the DNA polymerase delta subunit, Pol31
    Niloofar Davoodi Vijeh Motlagh
    Molecular Cell Biology Laboratory, Graduate School of Pharmaceutical Sciences, Tohoku University, Aoba 6 3, Sendai, Miyagi 980 8578, Japan
    DNA Repair (Amst) 5:1459-74. 2006
    ..We also demonstrate that Mgs1 interacts physically with Pol31 in vivo. Moreover, regions I and VII of Pol31, which are specifically sensitive to high levels of Mgs1 and PCNA, could be sites of interaction...
  20. ncbi Rad18/Rad5/Mms2-mediated polyubiquitination of PCNA is implicated in replication completion during replication stress
    Dana Branzei
    Molecular Cell Biology Laboratory, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, 980 8578, Japan
    Genes Cells 9:1031-42. 2004
    ..Our results are consistent with the idea that the Rad18/Rad5/Mms2 polyubiquitination pathway is important for replication completion, perhaps by promoting a template switch type of DNA synthesis...
  21. ncbi Ubc9 is required for damage-tolerance and damage-induced interchromosomal homologous recombination in S. cerevisiae
    Daisuke Maeda
    Molecular Cell Biology Laboratory, Graduate School of Pharmaceutical Sciences, Tohoku University, Aoba, Aramaki, Aoba-ku, Sendai 980-8578, Japan
    DNA Repair (Amst) 3:335-41. 2004
    ....
  22. ncbi Characterization of the slow-growth phenotype of S. cerevisiae Whip/Mgs1 Sgs1 double deletion mutants
    Dana Branzei
    Molecular Cell Biology Laboratory, Graduate School of Pharmaceutical Sciences, Tohoku University, Aoba ku, Sendai, Miyagi, Japan
    DNA Repair (Amst) 1:671-82. 2002
    ..Our results suggest that Whip/Mgs1 is implicated in DNA metabolism, and is required for normal growth and cell cycle progression in the absence of Sgs1...