Universitą degli studi di Pavia


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Pignataro's curriculum

Curriculum Vitae

Personal informations
Daniela Pignataro, born in Melzo (MI)on November 3th, 1985. Address: via Cimabue 17/12 - 20096 Pioltello (MI).
Laboratory address: Molecular Genetics Institute of the National Reaserch Council (MGI-NRC) – Via Abbiategrasso 207 - 27100 Pavia - Italy. Tel: 0382/546374
Email: pignataro@igm.cnr.it

Study background:
November 2012. XXVIII cycle PhD Student in Genetics and Molecular Biology at Molecular Genetics Institute of the NRC, Pavia. University of Pavia.
Supervisor: Prof. Giuseppe Biamonti.

February – October 2012. Research Fellow at Molecular Genetics Institute of the NRC, Pavia.
Aim of the study: Role of alternative splicing in tumoral progression.

March – February 2011. Fellowship at Italian Auxological Institute, Cusano Milanino.
Aim of the study: Genetic screening of patients with suspected Rett Syndrome.

March 2011. Master Degree in Molecular Biology at University of Milano - Bicocca.
Experimental graduation thesis: “Molecular characterization of a clinically heterogeneous cohort of patients with Cornelia de Lange syndrome: a study of candidate genes and search for rearrangements by array-CGH”.
Supervisor: Prof. Silvia Nicolis
Co-supervisor: Dr. Silvia Russo
April 2008. Bachelor’s Degree in Biological Sciences at University of Milano - Bicocca.
Graduation thesis: “Effect of particulate air pollution on A549 pulmonary alveolar cell line”.
Supervisor: Prof. Marina Camatini
Co-supervisor: Dr. Paride Mantecca


Attendance at conference

2012. 1st Post-EURASNET Symposium “Regulation of Gene Expression through RNA Splicing”, March 24-27 Trieste.
2011. Convegno nazionale AIR “Dalla diagnosi alla presa in carico delle disabilitą complesse: il modello della Sindrome di Rett”, Genova 11-12 Giugno.

Research project

Analysis of splicing factors in a cellular model of Alzheimer’s Disease

Alzheimer's disease (AD) is the most common neurodegenerative disease accounting for 60% of all dementia. Two features are commonly found in the AD brain: intraneuronal neurofibrillary tangles (NFTs) and extracellular neuritic plaques (NPs); these features are found to be present in the temporal neocortex and hippocampal region of the AD brain. NPs are composed by the beta amyloid peptide (Aβ peptide) while NFTs result from hyperphosphorylated or/and alternative splicing of microtubule-associated protein tau. Microtubule-associated tau proteins are nervous system-specific, they facilitates in microtubule assembly and the stabilization of microtubule polymers; both alternative splicing and phosphorylation of tau have been shown to regulate microtubule stability. In AD the amount of microtubule-bound tau protein isoform is reduced since the isoforms aggregate into NFTs, resulting in microtubule instability and in cell death.
An in vitro model to study neurodegenerative disorders is based on the human neuroblastoma SH-SY5Y cell line which can be induced to differentiate into a functionally mature neuronal phenotype.
A number of data in the literature suggest that both NFTs and NPs are induced by stressing agents such as hypoxia. These agents are known to perturb alternative splicing profiles by modulating the level and activity of splicing regulators.
The aim of my project is to investigate the link between neurodegeneration and alternative splicing. I will investigate by RNA seq the perturbation of splicing profiles and of the expression level of splicing factors in differentiated SH-SY5Y cells treated with the beta amyloid peptide or subjected to stressing stimuli, first of all hypoxia.

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