Ph.D., 1995, University of Padua, Italy
Research Interests
Aberrant DNA replication is one of the leading causes of mutations and chromosome rearrangements associated with several cancer related pathologies, and several chemotherapeutic strategies employ agents that induce replication stress in the attempt to selectively target highly proliferating cancer cells. Our group studies the mechanisms that operate in eukaryotic cells to maintain replication fork integrity. In particular, we use a combination of cellular, biochemical and structural approaches to define the role of RecQ helicases in this process. Our recent studies provided new mechanistic insight into the role of RecQ helicases in replication stress response, offering new molecular perspectives to potentiate chemotherapeutic regimens based on replication inhibitor treatment.
Recent Publications
  • RECQ1 helicase-driven DNA unwinding, annealing, and branch migration: insights from DNA complex structures.
    Pike ACW, Gomathinayagam S, et al. Proc Natl Acad Sci USA. (2015), in press.
  • Rad51-mediated replication fork reversal is a global response to genotoxic treatments in human cells.
    Zellweger R, Dalcher D, et al. J Cell Biol. (2015) 208(5):563-579.
  • DNA2 drives processing and restart of reversed replication forks in human cells.
    Thangavel S, Berti M, et al. J Cell Biol. (2015) 208(5):545-562.
  • Identification of RECQ1-regulated transcriptome uncovers a role of RECQ1 in regulation of cancer cell migration and invasion.
    Li XL, Lu X, et al. Cell Cycle. (2014) 13(15):2431-2445.

Full list of publications in PubMed: Vindigni A