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ELENA ZIVIANI

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Position

Professoressa Associata

Address

VIA U. BASSI, 58/B - PADOVA

Telephone

0498276237

Education
2006 Doctor of Philosophy in Neuroscience, Faculty of Medicine and Biological Sciences, Leicester University (UK), (Supervisor: Professor Pierluigi Nicotera).
2001 Laurea degree in Biological Sciences, University of Padua (Italy). Final score: 110/110
Research and Professional Experience
2017-present: Associate Professor of Biochemistry, Department of Biology, University of Padua, Italy.
2014-2017: Assistant Professor of Biochemistry, Giovani Ricercatori “Rita Levi Montalcini”, Department of Biology, University of Padua, Italy.
2012-2014: Boursieres d’Excellence, Marie Curie Action Fellow. Faculté de médecine de Genève, University of Geneva, Switzerland.
2011-2012: Boursieres d’Excellence, EMBO long term Fellow. Faculté de médecine de Genève, University of Geneva, Switzerland.
2007-2011: Post Doctoral scientist. Medical Research Council (MRC), Centre for developmental and biomedical genetics. UK, Sheffield. (Neuroscience, Prof. A. Whitworth).
2006-2007: Post Doctoral scientist. Medical Research Council (MRC), Toxicology Unit. UK, Leicester. (Neuroscience, Prof. P. Nicotera).
2001-2006: PhD Student. Medical Research Council (MRC), Toxicology Unit. UK, Leicester (Neuroscience, Prof. P. Nicotera).
Research Support
2024
1. Michael J Fox Foundation (USA); Spring 2024 RFP; 199,376.80 $
Role: PI
Duration: 1.5 years (18 months)
2. Parkinson’s Disease Foundation (USA); Impact Award; 150,000 $
Role: PI
Duration: 1 year (12 months)

Notices

Office hours

  • at Dipartimento di Biologia, Complesso Vallisneri, sesto piano NORD, lab numero 59
    RIceve previo appuntamento al 045 827 6237

Publications

Selected Peer-reviewed Publications
Research Articles
1. Mitochondrial quality control beyond PINK1/Parkin.
von Stockum S, Marchesan E, Ziviani E.
Oncotarget. 2018 9:12550-12551.
2. Postranslational modification of Parkin.
Chakraborty J., Basso V. and Ziviani E.
Biology Direct. Accepted. (2017)
3. The organelle replication connection
Ziviani E. and Scorrano L.
Nature. 538:326-327. (2016)
4. Mitochondrial dynamics and mitophagy in Parkinson's disease: A fly point of view.
Stockum S, Nardin A, Schrepfer E, Ziviani E.
Neurobiol Dis. 90:58-67. (2016)
5. Counteracting PINK/Parkin deficiency in the activation of mitophagy: a potential therapeutic intervention for Parkinson's Disease.
Nardin A, Schrepfer E, Ziviani E.
Curr Neuropharmacol. 14:250-9. (2016)
6. Parkinsonian toxin-induced oxidative stress inhibits basal autophagy in astrocytes via NQO2/quinone oxidoreductase 2: Implications for neuroprotection.
Janda E, Lascala A, Carresi C, Parafati M, Aprigliano S, Russo V, Savoia C, Ziviani E, Musolino V, Morani F, Isidoro C, Mollace V.
Autophagy. 11:1063-80 (2015)
7. Genome-wide RNAi screen identifies the Parkinson disease GWAS risk locus SREBF1 as a regulator of mitophagy.
Ivatt RM, Sanchez-Martinez A, Godena VK, Brown S, Ziviani E, Whitworth AJ.
Proc Natl Acad Sci U S A. 111:8494-9. (2014)
8. Reduction of endoplasmic reticulum stress attenuates the defects caused by Drosophila mitofusin depletion.
Debattisti V, Pendin D, Ziviani E, Daga A, Scorrano L.
J Cell Biol. 204:303-12. (2014)
9. In Epiepsy, BAD is not really bad.
Ziviani E and Scorrano L
Neuron. 74:600-2. (2012)
10. Ryanodine receptor-2 upregulation and nicotine-mediated plasticity.
Ziviani E, Lippi G, Bano D, Munarriz E, Guiducci S, Zoli M, Young KW, Nicotera P.
EMBO J. 30:194-204. (2011)
11. Analysing the role of the PINK1/Parkin pathway in Mitophagy
Rachael I, Ziviani E and Whitworth AJ.
Journal of Neurogenetic. 24: 57-57. (2010)
12. How could Parkin-mediated ubiquitination of mitofusin promote mitophagy?
Autophagy. 6:660-2. (2010)
13. Drosophila Parkin requires PINK1 for mitochondrial translocation and ubiquitinates Mitofusin
Ziviani E, Tao RN, Whitworth AJ.
Proc Natl Acad Sci U S A. 107:5018-23. (2010)
14. Modulation of mitochondrial function and morphology by interaction of Omi/HtrA2 with the mitochondrial fusion factor OPA1
Kira M. Holmström, Nicole Kieper, Dalila Ciceri, Fabienne C. Fiesel, Ziviani E, Alexander J. Whitworth, Hartwig Wolburg, L. Miguel Martins, Philipp J. Kahle, Rejko Krüger
Exp Cell Res. 316:1213-24. (2010)
15. Rapamycin activation of 4E-BP prevents parkinsonian dopaminergic neuron loss
Tain LS, Mortiboys H, Ziviani E, Tao RN, Bandmann O, Whitworth AJ.
Nat Neurosci. 12:1129-35. (2009)
16. The plasma membrane Na+/Ca2+ exchanger is cleaved by distinct protease families in neuronal cell death.
Bano D, Munarriz E, Chen HL, Ziviani E, Lippi G, Young KW, Nicotera P.
Ann N Y Acad Sci. 1099:451-5. (2007)





Research Area

Dr Elena Ziviani has a broad background in Neuroscience, with specific training and expertise in molecular biology, in vitro primary neuron culture and in vivo experimentation, both in mice and in Drosophila Melanogaster fruit fly. Dr Ziviani accomplished her PhD in Neuroscience at the MRC toxicology Unit in Leicester, UK, under the supervision of Professor P. Nicotera where Elena investigated the effect of nicotine in primary neurons on neuroprotection and synaptic plasticity. In November 2007, Dr Ziviani joined Dr. Alex Whitworth’s group in Sheffield, UK, where she studied the role of Parkinson’s Disease (PD)-related proteins PINK1 and Parkin in mitochondrial dynamic and mitophagy, using Drosophila Melanogaster as a neurodegenerative disease model as well as fibroblast cells from PD patients. In this work, she unrevealed the biochemical link between PINK1/Parkin pathway and mitochondrial pro-fusion protein Mitofusin (MFN). In December 2010 Dr Ziviani was awarded with both EMBO long term and Marie Curie Action fellowships. Since 2014 she became independent PI c/o department of Biology at the University of Padova where. Ziviani's lab is interested in the molecular pathway leading to neurodegeneration specifically in the context of PD and mitochondria dysfunction. Mitochondrial dysfunction has become a central theme in neurodegenerative diseases, in particular PD. However more work is required to bring mitochondria forward as a therapeutic target in PD. We postulate that while mitochondria communicate with other organelles, impairments of these interorganellar interactions (particularly ER-mitochondria crosstalk) are pivotal for PD onset and progression.

Thesis proposals

Mitochondrial dysfunction has become a central theme in neurodegenerative diseases, in particular Parkinson’s Disease (PD). NF-kB factors are cardinal transcriptional regulators of inflammation and apoptosis and have been involved in the brain programming of systemic aging as well as in the pathogenesis of several neurodegenerative diseases, including PD. In particular, mice deficient for the c-Rel subunit develop with aging a L-DOPA-responsive parkinsonism associated with loss of dopaminergic (DA) neurons in the substantia nigra, neuroinflammation and accumulation of alpha-synuclein and iron. Parkin, a PD gene and an E3 ubiquitin ligase that regulates mitochondria quality control, upregulates the mitochondrial fusion protein OPA1 through linear ubiquitination of NF-kB essential modulator (NEMO), which is pivotal for the activation of canonical NF-kB pathway. Relevantly, patients with two close OPA1 missense mutations (p.G488R, p.A495V) leading to age-dependent syndromic parkinsonism and dementia have been reported, substantiating a role for OPA1 dysfunction in DA neurons pathology, which is further sustained by the evidence that moderate overexpression of OPA1 is beneficial in primary mitochondrial disease mice model with respectively complex I and IV deficiency. Considering the described scenario, this project hypothesizes that normalizing OPA1 expression levels ameliorates the parkinsonism associated with c-rel/NF-kB deficient mouse. Should impaired OPA1 expression affect mitochondria function in c-rel/NF-kB deficient mice, we expect that normalizing OPA1 levels will contribute to ameliorate the PD phenotypes associated with c-rel/NF-kB mouse, presumably by increasing mitochondrial respiratory efficiency, blunting cytochrome c release and reactive oxygen species production, and exerting cell protection from death. This study will ultimately clarify the role of OPA1 as a crossroad of the above described pathways regulating mitochondrial function, and it will contribute to bring mitochondria forward as a therapeutic target in PD.