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
  • 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.
  • Discovery of ML216, a small molecule inhibitor of Bloom (BLM) helices.
    Rosenthal AS, Dexheimer TS, et al. Probe Reports from the NIH Molecular Libraries Program [Internet]. Bethesda (MD): National Center for Biotechnology Information (US). (updated 2013 Feb 28).
  • The two faces of DNA repair: disease and therapy.
    Vindigni A, Gonzalo S. Mo Med. (2013) 110(4):314-319.
  • Bioinformatic analysis of RecQ4 helicases reveals the presence of a RQC domain and a Zn knuckle.
    Marino F, Vindigni A, et al. Biophys Chem. (2013) 177-178:34-9.
  • Human RECQ1 promotes restart of replication forks reversed by DNA topoisomerase 1 inhibition.
    Berti M, Chaudhuri AR, et al. Nat Struct Mol Biol. (2013) 20(3):347-54.

Full list of publications in PubMed: Vindigni A