Academic position: Assistant Professor
Phone number: 0382 546331 (laboratory)/0382 546345 (office)
Fax: 0382 422286
Department: Department of Biology and Biotechnology “Lazzaro Spallanzani”
Graduated cum laude in Biological Sciences at the University of Pavia, she performed her PhD in Biological Science at the European Molecular Biology Laboratory (EMBL) of Heidelberg-Germany, under the supervision of Dr. R. Klein. She has been an EMBO long-term postdoctoral Fellow at the Institute of Molecular Genetics (IGM) CNR of Pavia and subsequently the Principal investigator of the Telethon research project “Identification of Rac3-interacting proteins during neuritogenesis”. Since 2003, she is member of the research unit leaded by Dr. M. Stefanini at the IGM CNR. The research is supported by the Italian Ministry of Education, University and Research (MIUR), the European Community, Cariplo Foundation and the Italian Association for Cancer Research (AIRC). Since September 2009 she is CNR researcher at the IGM CNR Pavia and leader of a research project sponsored by CNR/CNRS (2010-2011).
1999: Teaching contract at the University of Bologna (Scuola di Specialità in Genetica Applicata). 2005-2009: Teaching contract at the University of Pavia (Corso di Laurea Specialistica in Biologia Sperimentale Applicata).
Since 2010: Teaching contract at the University of Pavia (Corso di laurea Magistrale in Molecular Biology and Genetics).
She has extensive experience in the field of molecular biology and biochemistry, with special emphasis on nervous system development in mammals. During the PhD, she identified the in vivo function of several tyrosine kinase receptors during nervous system development by using the mouse gene targeting approach. Later on, her research has been focusing on the human syndromes xeroderma pigmentosum (XP), trichothiodistrophy (TTD) and Cockayne Syndrome (CS), which result from defects in nucleotide excision repair (NER), a versatile DNA repair system that removes a wide range of lesions, including UV photoproducts. The clinical features of these disorders are very different: XP is a highly cancer-prone disease, whereas TTD and CS are cancer-free multisystem disorders characterised by defects in physical and mental development, premature ageing and alterations in the immune and nervous systems. The photosensitive form of TTD is due to alterations in the XPB, XPD or TTDA genes that encode subunits of the repair/transcription complex TFIIH. By micro-array technology, she evaluated the gene expression profiles in primary fibroblasts from patients mutated in the XPD gene. This study allowed the identification of a limited number of “disease-specific” genes that are currently under investigation.