Eleonora was born and raised in the south of Italy until when, one day, she decided to left her region to look for better career opportunities. She enrolled in a Bachelor’s degree at the University of Camerino, Italy. She studied Nutritional Biology because she was always passionate about human biology and the effect of food on the human body.
During her studies, she discovered a new passion for molecular biology. She was attracted by the idea that DNA contains all the information that makes us human beings. She then worked on her Bachelor’s thesis in the genetic department of the Jilin Agricultural University in the north of China. The project aimed to clone sacB gene from B. Subtilis for the production of Levansucrase. There, she mastered many molecular techniques and she decided to pursue a career as a researcher.
Her hunger for knowledge pushed her to enroll in an interuniversity MSc program in Molecular Biology at VUB, KULeuven, and UAntwerp, in Belgium. During these two years, she had the possibility to broaden her knowledge of biology and to improve her skills in different techniques. She spent her last semester of study in Incheon, South Korea, where she worked under the supervision of Dr. Stefan Magez on characterizing the immune-destructive potential of Trypanosoma evansi infection on murine models.
After graduation, she has received a PhD position in the research institute Institut Necker Enfants Malades where she works on a TrainCDKs project, the identification of modifier genes for HNF1B kidney disease, under the supervision of Dr. Laurance Heidet and Dr. Marco Pontoglio.
Congenital Anomalies of Kidney and Urinary Tracts are often characterized by mutations in HNF1B gene. Interestingly, the same exact familial mutation can result in different phenotypic outcomes. We hypothesize that variants of modifier genes may influence HNF1B residual activity in hetherozygous patients, leading to a differential disease penetrance. Our goal is to reveal HNF1B modifier genes by performing a CRISPR/cas9 screening. This will lead to a better understanding of kidney diseases molecular pathway and hopefully, to the identification of drugs the can modulate HNF1B potency.