- Discovering Padova
- Il Bo
1991: Degree cum laude in Biological Sciences, University of Genova
1996: PhD Degree in Human Genetics, University of Torino
1998: Specialization Degree in Applied Genetics, University of Pavia
1991-1995 PhD student at the laboratory of Molecular Genetics of the Gaslini Institute, Genova, Italy.
1996-1999 Post doctoral fellow at the laboratory of Cellular and Molecular Immunology, INSERM U364, Nice, France.
1999-2005 Post doctoral fellow at the Institute for Cancer Research and Treatment, Candiolo, Torino, Italy.
From 2005 Assistant Professor in the Department of Biomedical Sciences, University of Padova, Italy.
From 2018 Associate Professor in the Department of Biomedical Sciences, University of Padova, Italy.
1. Changes in mitochondrial energy metabolism during neoplastic transformation, with a particular focus on tumors caused by the genetic syndrome neurofibromatosis type I.
2. Analysis of the role played by the mitochondrial chaperone TRAP1 in the tumorigenic process.
3. Mitochondrial kinases in survival and metabolic rewiring of tumor cells.
4. Study of the regulatory mechanisms and of the apoptotic role of the mitochondrial permeability transition pore (PTP) in neoplastic models.
Masgras I, Ciscato F, Brunati AM, Tibaldi E, Indraccolo S, Curtarello M, Chiara F, Cannino G, Papaleo E, Lambrughi M, Guzzo G, Gambalunga A, Pizzi M, Guzzardo V, Rugge M, Vuljan SE, Calabrese F, Bernardi P, Rasola A (2017) Absence of neurofibromin induces an oncogenic metabolic switch via mitochondrial ERK-mediated phosphorylation of the chaperone TRAP1. Cell Reports 18:659-672
Kowalik MA, Guzzo G, Morandi A, Perra A, Menegon S, Masgras I, Trevisan E, Angioni MM, Fornari F, Quagliata L, Ledda-Columbano GM, Gramantieri L, Terracciano L, Giordano S, Chiarugi P, Rasola A, Columbano A (2016) Metabolic reprogramming identifies the most aggressive lesions at early phases of hepatic carcinogenesis. Oncotarget 7:32375-32393
Guzzo G, Sciacovelli M, Bernardi P, Rasola A (2014) Inhibition of succinate dehydrogenase by the mitochondrial chaperone TRAP1 has anti-oxidant and anti-apoptotic effects on tumor cells. Oncotarget 5:11897-11908
Rasola A, Bernardi P (2014) The mitochondrial permeability transition pore and its adaptive responses in tumor cells. Cell Calcium 56:437-445
Rasola A, Picard D, Neckers L (2014) Mitochondrial oxidative phosphorylation TRAP(1)ped in tumor cells; Trends Cell Biol 24:455-463
Pantic B, Trevisan E, Citta A, Rigobello MP, Marin O, Bernardi P, Salvatori S, Rasola A (2013) Myotonic dystrophy protein kinase (DMPK) prevents ROS-induced cell death by assembling a hexokinase II-Src complex on the mitochondrial surface Cell Death Dis 4:e858
Sciacovelli M, Guzzo G, Morello V, Frezza C, Zheng L, Nannini N, Calabrese F, Laudiero G, Esposito F, Landriscina M, Defilippi P, Bernardi P, Rasola A (2013) The mitochondrial chaperone TRAP1 promotes neoplastic growth by inhibiting succinate dehydrogenase. Cell Metab 17:988-999
Rasola A, Sciacovelli M, Chiara F, Pantic B, Brusilow WS, Bernardi P (2010) Activation of mitochondrial ERK protects cancer cells from death through inhibition of the permeability transition. Proc Natl Acad Sci USA 107:726-731
Rasola A, Sciacovelli M, Pantic B, Bernardi P (2010) Signal transduction to the permeability transition pore. FEBS Lett 584:1989-1996
Chiara F, Castellaro D, Marin O, Petronilli V, Brusilow WS, Juhaszova M, Sollott SJ, Forte M, Bernardi P, Rasola A (2008) Hexokinase II Detachment from Mitochondria Triggers Apoptosis through the Permeability Transition Pore Independent of Voltage-Dependent Anion Channels. PLoS ONE 3:e1852
AIRC (Italian Association for Cancer Research)
University of Padova
Children’s Tumor Foundation
Neurofibromatosis Therapeutic Acceleration Program