Development of Citron Kinase as a therapeutic target for brain tumors.
2019-2024 | Italian Association for Cancer Research (AIRC)
Ferdinando Di Cunto, Principal Investigator
The aim of this project is to develop new strategies for inhibiting CITK. We have previously demonstrated that this protein is a potential target for treating medulloblastomas, aggressive brain tumors affecting mostly the cerebellum and the childhood.
Implementation of cellular and genetic models for validating genomic variants associated with neurodegenerative disorders.
2019-2021 | Fondazione CRT (Turin)
Ferdinando Di Cunto, Principal Investigator
The aim of this project is to develop new high throughput cellular and C. elegans models for the functional study of mutations identified in patients affected by neurogenetic disorders.
Identification and initial validation of new possible treatments for intellectual disability in Down syndrome through drug repositioning
2017-2019 | Fondation Jerome Lèjeune (Paris)
Ferdinando Di Cunto, Principal Investigator
The aim of this project is to identify new potential therapies for Down syndrome, using bioinformatics drug repositioning and validation in cultured neuronal models.
Validation of Citron kinase as a therapeutic target for medulloblastoma
2015-2018 | Italian Association for Cancer Research (AIRC)
Ferdinando Di Cunto, Principal Investigator
The aim of this project is to establish whether the microcephaly protein Citron kinase is a useful target for treating medulloblastomas, aggressive brain tumors affecting mostly the cerebellum and the childhood.
Relevance of the axonal SMN protein (a‐SMN) for spinal muscular atrophy: novel cell models, transgenic mice and therapeutic approaches
2013-2017 | Telethon Foundation
Ferdinando Di Cunto, Unit Leader; Giorgio Battaglia, Besta Neurological Institute, Milan, Principal Investigator
The aim of this project is to address whether aSMN, an alternative splicing product of the SMN gene that potently stimulates axonal outgrowth, is capable of compensating for SMN loss in spinal muscular atrophy disease models.
Disruption of circadian rhythms and epigenetic modifications in D. melanogaster
2013-2018 | CNR, Epigen flagship project
Ferdinando Di Cunto, Unit Leader; Rodolfo Costa, University of Padova, Principal Investigator
The aim of this project is to understand the molecular alterations produced by shift-work in a Drosophila model. The role of the unit is to perform the bioinformatical analysis of gene expression data.
Identification of therapeutic targets in primary microcephaly through the analysis of the CIT-K/ASPM pathway
2012-2015 | Telethon Foundation
Ferdinando Di Cunto, Principal Investigator
The aim of this project is to investigate the molecular relationships between the two microcephaly proteins Citron kinase and ASPM, and to understand the molecular mechanisms by which the absence of Citron kinase leads to the death of neuronal progenitors during CNS development.
Functional analysis of the DSCR gene TTC3 in neuronal differentiation and in a Down syndrome mouse model
2012-2014 | Fondation Jerome Lèjeune (Paris)
Ferdinando Di Cunto, Principal Investigator
The aim of this project is to characterize the role palyed in Down syndrome by TTC3, one of the Chromosome 21 genes whose expression is more altered in DS patients and in DS mouse models.
Molecular characterization of TDP-43 function in vivo and the mechanisms that lead to motoneuron disease in Drosophila models of ALS
2011-2013 | ARISLA
Ferdinando Di Cunto, Unit Leader; Fabian Feiguin, ICGEB, Trieste, Principal Investigator
The aim of this project is to characterize the molecular changes produced in Drosophila by the loss of TBPH, the homologue of ALS gene TDP-43. The role of the unit is to perform the bioinformatica analysis of gene expression data.
Motor neuron death in Spinal Muscular Atrophy (SMA) : new animal models and innovative therapeutic strategies
2011-2015 | Italian Ministry of Health
Ferdinando Di Cunto, Unit Leader; Giorgio Battaglia, Besta Neurological Institute, Milan, Principal Investigator
The aim of this project is to address whether aSMN, an alternative splicing product of the SMN gene that potently stimulates axonal outgrowth, is capable of compensating for SMN loss in spinal muscular atrophy disease models.
