Assistant Professor

University of Trieste

Molecular Oncology Unit, LNCIB Trieste

fiamma.mantovani@lncib.it

Dr. Fiamma Mantovani received her BSc in Biology in 1994 at the University of Trieste, and her PhD in Molecular Genetics in 2002 at SISSA-ISAS, Trieste. Since 2008 she is Assistant Professor in Applied Biology at the University of Trieste, Department of Life Sciences.

Since the beginning of her scientific career in the group of L. Banks (ICGEB), dr. Mantovani has been studying the regulation of the p53 tumor suppressor. Upon joining the Molecular Oncology group directed by G. Del Sal at LNCIB, she has highlighted several mechanisms that transduce stress signaling to both transcription-dependent and extranuclear apoptotic activities of p53. Her interests also span the mechanisms of unscheduled activation of p53 in Huntington’s Disease, to identify hubs amenable to therapeutic intervention. Her current research interests are focused on how the mechanisms of transcription regulation are altered during tumor progression and neurodegeneration, with particular focus on the roles of chromatin remodeling regulators and noncoding RNAs.

Recent publications:

• Mantovani F, Zannini A, Rustighi A, Del Sal G. Interaction of p53 with prolyl isomerases: Healthy and unhealthy relationships. (2015) Biochim Biophys Acta. pii: S0304-4165(15)00033-1.

• Bitomsky N, Conrad E, Moritz C, Polonio-Vallon T, Sombroek D, Schultheiss K, Glas C, Greiner V, Herbel C, Mantovani F, Del Sal G, Peri, F, Hofmann T G. Autophosphorylation and Pin1 binding coordinate DNA damage-induced HIPK2 activation and cell death. (2013) Proc Natl Acad Sci U S A 110: E4203-E4212.

• Sorrentino G, Mioni M, Giorgi C, Ruggeri N, Pinton P, Moll U, Mantovani F, Del Sal G. The prolyl-isomerase Pin1 activates the mitochondrial death program of p53. (2012) Cell Death Differ 20: 198-208.

• Grison A*, Mantovani F*, Comel A, Agostoni E, Gustincich S, Persichetti F, Del Sal G. Ser46 phosphorylation and prolyl-isomerase Pin1-mediated isomerization of p53 are key events in p53-dependent apoptosis induced by mutant huntingtin. (2011) Proc Natl Acad Sci U S A: 17979-84. * Equal contribution

• Drost J*, Mantovani F*, Tocco F, Elkon R, Comel A, Holstege H, Kerkhoven R, Jonkers J, Voorhoeve PM, Agami R, Del Sal G. BRD7 is a candidate tumour suppressor gene required for p53 function. (2010) Nat Cell Biol. 12:380-9. * Equal contribution