University College London, London, England, BSc Biochemistry, 1992
University of London, London, England, PhD, 2000
Since 2018, Group Leader, RNA Biology Group, ICGEB, Trieste, Italy
2013-2017, Group Leader, Biotechnology Development Group, ICGEB, Trieste, Italy
2003-2013, Research Scientist, Biotechnology Development Group, ICGEB, Trieste, Italy
Since beginning his postdoctoral work Dr. Baralle’s interests have been the role of RNA splicing in genetic disease with particular interest in how in the mechanism of splicing is affected by gene mutations, what this teaches us about the complex mechanism and role of splicing. Uniting his 5 years as head of the Biotechnology group, where he concentrated on Biological proteins of Pharmaceutical interest, he focuses on how the knowledge of these mechanisms can be used to prevent or alter disease.
Polez, S., Origi, D., Zahariev, S., Guarnaccia, C., Tisminetzky, S.G., Skoko, N. and Baralle, M. (2016) A Simplified and Efficient Process for Insulin Production in Pichia pastoris. PloS one, 11, e0167207.
De Conti, L., Akinyi, M.V., Mendoza-Maldonado, R., Romano, M., Baralle, M. and Buratti, E. (2015) TDP-43 affects splicing profiles and isoform production of genes involved in the apoptotic and mitotic cellular pathways. Nucleic acids research, 43, 8990-9005.
Bembich, S., Herzog, J.S., De Conti, L., Stuani, C., Avendano-Vazquez, S.E., Buratti, E., Baralle, M. and Baralle, F.E. (2014) Predominance of spliceosomal complex formation over polyadenylation site selection in TDP-43 autoregulation. Nucleic acids research, 42, 3362-3371.
Buratti, E., Baralle, M. and Baralle, F.E. (2013) From single splicing events to thousands: the ambiguous step forward in splicing research. Briefings in functional genomics, 12, 3-12.
Ayala,Y.M., De Conti,L., Avendaño-Vázquez,S.E., Dhir,A., Romano,M., D’Ambrogio,A., Tollervey,J., Ule,J., Baralle,M., Buratti,E., et al. (2011) TDP-43 regulates its mRNA levels through a negative feedback loop. EMBO J., 30, 277–288
Zubovic, L., Baralle, M. and Baralle, F.E. (2012) Mutually exclusive splicing regulates the Nav 1.6 sodium channel function through a combinatorial mechanism that involves three distinct splicing regulatory elements and their ligands. Nucleic acids research, 40, 6255-6269.
Nuzzo,F., Radu,C., Baralle,M., Spiezia,L., Hackeng,T.M., Simioni,P. and Castoldi,E. (2013) Antisense-based RNA therapy of factor V deficiency: in vitro and ex vivo rescue of a F5 deep-intronic splicing mutation. Blood, 122, 3825–3831.