10/1998: B.S. degree cum laude- University of Milan. Thesis: “Chromatin structure of urokinase gene”. Lab. of Prof. F. Blasi, DIBIT- HSR, Milan.
1998-1999: Telethon Fellow- University of Milan. Lab. of Prof. R. Mantovani.
02/2003: PhD awarded in Biotechnology and Molecular Medicine, University of Modena and Reggio Emilia. Thesis: “Regulation of NF-Y activity by coactivators and corepressors: HSP-CBF and p53”.
2002-2005: Post-doc.-University of Modena and Reggio Emilia. Fellowship from Fondazione Italiana Ricerca sul Cancro (FIRC). Lab. of Prof. R. Mantovani.
11/2005-current: Research Assistant Professor of Genetics-Department of Biology, University of Modena and Reggio Emilia.
2006-current: Member of the College of Education of the PhD Program in Evolutionary Biology-University of Modena and Reggio Emilia.
2009-current: Member of the College of Education of the PhD Program in Molecular and Regenerative Medicine-University of Modena and Reggio Emilia.

Cell cycle progression is regulated by finely tuning the expression and the activity of various key proteins. The transcriptional control of cell cycle regulators is one of the main mechanisms through which the cell proceeds properly through the different phases of the cell cycle. The CCAAT-binding factor NF-Y is a mammalian transcription factor that binds to CCAAT boxes in the promoters of a wide variety of genes, among which cell cycle-regulatory genes. Bioinformatic analyses of cell cycle promoters showed a remarkable and specific abundance of CCAAT boxes in promoters regulated during the G2/M phase. NF-Y is a heterotrimeric complex composed of three subunits, A, B, and C, which are all essential for CCAAT binding. NF-YB and NF-YC dimerization is essential for NF-YA association and sequence-specific DNA binding. The three subunits are regulated at different levels. NF-YA has two major isoforms generated by alternative splicing, variously expressed in different cell types. NF-YC also has different isoforms that are regulated in a cell-specific way, while NF-YB has only one splice variant. NF-Y is required to organize the chromatin in proximity of transcriptional start sites, thereby enabling recruitment of coactivators. It is also involved in the modulation of the activity of cell cycle promoters in response to DNA damage, through wild-type p53-dependent transcriptional inhibition. Mutant p53/NF-Y complexes have the opposite effect on transcription upon DNA damage, that is, transactivation of proliferative genes and aberrant cell cycle regulation. Genome wide mRNA expression profiling of the transformation process verified that p53-mediated transcriptional repression of several targets is dependent on the activities of NF-Y, p21 and E2F.
The main interest of our laboratory is to shed light on the specific role of NF-Y in cell cycle regulation. We are studying the effect on cell viability and cell cycle progression of the selective knock-down of each NF-Y subunit through RNAi. Moreover we are investigating the role of NF-Y in balancing the apoptotic activity of p53 upon DNA damage or stress stimuli.
In the last years we have expanded our studies to the molecular activity of new anti-proliferative agents, derived from the natural polyphenol Curcumin, which has demonstrated chemotherapeutic and chemopreventive activity. In particular we are investigating their effect on key cell cycle genes, among which NF-Y and p53, and their activity as anti-tumor epigenetic drugs.

·Benatti P, Dolfini D, Viganò A, Ravo M, Weisz A, Imbriano C. (2011) Specific inhibition of NF-Y subunits triggers different cell proliferation defects. Nucleic Acids Research, in press.
·Caporuscio F., Rastelli G., Imbriano C., Del Ri A. (2011). Structure-based design of potent aromatase inhibitors by high-throughput docking. J Med Chem 54(12): 4006-17.
·Caselli M., Ferrari E., Imbriano C., Pignedoli F., Saladini M., Ponterini G. (2010). Probing solute–solvent hydrogen bonding with fluorescent water-soluble curcuminoids, J. Photochem. Photobiol. A: Chem, doi:10.1016/j.photochem.2010.01.008.
·Basile V., Ferrari E., Lazzari S., Belluti S., Pignedoli F., and Imbriano C. (2009). Curcumin derivatives: molecular basis of their anti-cancer activity. Biochemical Pharmacology, 78(10):1305-15.
·Ceribelli M., Benatti P., Imbriano C., Mantovani R. (2009) NF-YC complexity is generated by dual promoters and alternative splicings. J Biol. Chem., 284(49):34189-200.
·Benatti P., Basile V., Merico D., Fantoni L.I., Tagliafico E.,and Imbriano C. (2008). A balance between NF-Y and p53 governs the pro- and anti-apoptotic transcriptional response. Nucleic Acids Research, 36(5):1415-28.
·Donati G., Imbriano C. and Mantovani R. (2006). Dynamic recruitment of transcription factors and epigenetic changes on the ER stress response gene promoters. Nucleic Acid Res., 34(10):3116-27.
·Basile V., Mantovani R. and Imbriano C. (2006). DNA-damage promotes HDAC4 nuclear localization and G2/M promoters repression via p53 C-terminal lysines, J Biol. Chem., 281(4):2347-57.
·Imbriano C., Gurtner A., Cocchiarella F., Di Agostino S., Basile V., Gostissa M., Dobbelstein M., Del Sal G., Piaggio G., Mantovani R. (2005). Direct p53 transcriptional repression: in vivo analysis of CCAAT-containing G2/M promoters, Mol Cell Biol. 25(9):3737-51.

No projects are available to students for the current accademic year.