Universitą degli studi di Pavia
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Di Maio's curriculum
Curriculum
Personal Information
Name Antonina Di Maio
Adress Via Felice Cavallotti n 30 Castelvetrano (TP)
Telephone 3280715154
E-mail antonina.dimaio01@ateneopv.it
Nazionality Italiana
Date of birth 27/03/1989
Education and Training
01/11/2014 – Present
PhD Program in “Genetics, Molecular and Cellular Biology”, University of Pavia, XXX cycle (2014/2017). Supervisor: Dr.Alessandra Montecucco.
10/10/2012 – 24/07/2014
Master Degree in "Experimental and Applied Biology" (Curriculum: “Human Biology and Biomedical Sciences), University of Pavia, Italy.”. Thesis: “Studio di modificazioni istoniche in cellule DNA Ligasi I difettive”. Supervisor: Dr. Alessandra Montecucco. 110/110 cum laude.
13/10/2008 – 18/07/2012
Bachelor Degree in "Biological Sciences", University of Palermo, Italy. . Thesis: “La produzione di piastrine pathogen free destinate ai pazienti immunocompromessi”. Supervisor: Dr. Elena Carra. 95/110.
15/07/2008
Diploma di scuola superiore, Liceo Scientifico Michele Cipolla, Castelvetrano (TP), Italia. 91/100.
Professional qualifications
- Computer skills; I attained European Computer Driving Licence (ECDL) in 2008.
- Laboratory skills; Eukaryotic cell culture; Western blotting, Western Blotting 2D, ChIP seq
Publications
Research project
Response to DNA damage and organization of the cytoskeleton in cell models of chronic stress
The DNA damage is a significant threat for the stability of genome and chromatin organization. Whereas the majority of men are exposed to low levels of DNA damaging agents, whether endogenous and exogenous, the response to low doses of damage is crucial for establishing the environmental risk factors for the development of tumors. During the studies conducted on our cellular model of chronic stress, we observed subtle morphological differences between cells with DNA damage and their respective controls. We therefore assume that the change in cell morphology is due to DNA damage. Our hypothesis is that a modest DNA damage might affect the phenotype and cell motility, and therefore have a role in the metastasis of cancer cells.
Personal Information
Name Antonina Di Maio
Adress Via Felice Cavallotti n 30 Castelvetrano (TP)
Telephone 3280715154
E-mail antonina.dimaio01@ateneopv.it
Nazionality Italiana
Date of birth 27/03/1989
Education and Training
01/11/2014 – Present
PhD Program in “Genetics, Molecular and Cellular Biology”, University of Pavia, XXX cycle (2014/2017). Supervisor: Dr.Alessandra Montecucco.
10/10/2012 – 24/07/2014
Master Degree in "Experimental and Applied Biology" (Curriculum: “Human Biology and Biomedical Sciences), University of Pavia, Italy.”. Thesis: “Studio di modificazioni istoniche in cellule DNA Ligasi I difettive”. Supervisor: Dr. Alessandra Montecucco. 110/110 cum laude.
13/10/2008 – 18/07/2012
Bachelor Degree in "Biological Sciences", University of Palermo, Italy. . Thesis: “La produzione di piastrine pathogen free destinate ai pazienti immunocompromessi”. Supervisor: Dr. Elena Carra. 95/110.
15/07/2008
Diploma di scuola superiore, Liceo Scientifico Michele Cipolla, Castelvetrano (TP), Italia. 91/100.
Professional qualifications
- Computer skills; I attained European Computer Driving Licence (ECDL) in 2008.
- Laboratory skills; Eukaryotic cell culture; Western blotting, Western Blotting 2D, ChIP seq
Publications
Research project
Response to DNA damage and organization of the cytoskeleton in cell models of chronic stress
The DNA damage is a significant threat for the stability of genome and chromatin organization. Whereas the majority of men are exposed to low levels of DNA damaging agents, whether endogenous and exogenous, the response to low doses of damage is crucial for establishing the environmental risk factors for the development of tumors. During the studies conducted on our cellular model of chronic stress, we observed subtle morphological differences between cells with DNA damage and their respective controls. We therefore assume that the change in cell morphology is due to DNA damage. Our hypothesis is that a modest DNA damage might affect the phenotype and cell motility, and therefore have a role in the metastasis of cancer cells.
