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Content archived on 2024-06-16

Insights into novel therapeutic strategies for a nuclear inclusion disease caused by polyalanine expansion

Objective

A broad range of degenerative diseases is associated with intracellular inclusions formed by toxic, aggregation-prone mutant proteins. Intranuclear inclusions constitute a pathological hallmark of oculopharyngeal muscular dystrophy (OPMD), a rare inherited disease caused by (GCG) repeat expansions in the gene that encodes for nuclear poly(A) binding protein (PABPN1). The mutation results in an extended polyalanine stretch that has been proposed to induce protein aggregation and formation of intranuclear inclusions.

The participants in this Consortium have previously generated cellular and animal models for OPMD. The present proposal aims to make use of these models to study the molecular mechanisms of OPMD and to develop new strategies for its treatment.

Studies on the molecular mechanisms of OPMD will involve basic research on the structure and function of normal versus expanded PABPN1 protein and a determination of its interacting partners within the cell. The development of therapeutic strategies will include (i), screening for small molecules that can suppress the muscle phenotype in a Drosophila model of OPMD and (ii), the design of viral vectors for negating mutant PABPN1 function by means of siRNA-mediated knockdown or protein suppressors.

In parallel, a combined transcriptomic and metabonomic analysis will be performed on OPMD families. This knowledge will be essential to validate the data collected in the cellular and animal models and to provide potential biomarkers to monitor the direct effects of drug intervention, disease phenotype suppressors and gene therapy approaches.

Call for proposal

FP6-2004-LIFESCIHEALTH-5
See other projects for this call

Coordinator

INSTITUTE OF MOLECULAR MEDICINE
EU contribution
No data
Total cost
No data

Participants (5)