MITO BY-PASS POC
Molecular by-pass therapy for mitochondrial dysfunction - Proof of Concept
| Coordinatore | TAMPEREEN YLIOPISTO
Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie. |
| Nazionalità Coordinatore | Finland [FI] |
| Totale costo | 168˙224 € |
| EC contributo | 150˙000 € |
| Programma | FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013) |
| Code Call | ERC-2011-PoC |
| Funding Scheme | CSA-SA(POC) |
| Anno di inizio | 2012 |
| Periodo (anno-mese-giorno) | 2012-06-01 - 2013-05-31 |
Partecipanti
| # | ||||
|---|---|---|---|---|
| 1 |
TAMPEREEN YLIOPISTO
Organization address
address: Kalevantie 4 contact info |
FI (TAMPERE) | hostInstitution | 150˙000.00 |
Mappa
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Obiettivo del progetto (Objective)
'Defects in the primary metabolic functions of mitochondria, the cell’s ‘power-plants’, underlie a diverse range of human pathologies, including rare neuromuscular syndromes, many cases of common multifactorial diseases (e.g epilepsy, deafness, diabetes), neurodegenerative conditions such as Parkinson’s disease (PD), and devastating metabolic disorders of infancy. Mitochondrial dysfunction is also a major cause of tissue damage in heart attack and stroke, and is involved in cancer progression. This project will facilitate an R&D effort to develop a common genetic therapy for this vast range of diseases, taking advantage of the fact that lower organisms possess a built-in biochemical mechanism for relieving the stress caused by mitochondrial dysfunction, using alternative respiratory chain enzymes that simply by-pass the problem. Under ERC Project 232738 (MITO BY-PASS) we have succeeded in expressing the alternative oxidase AOX from the sea squirt Ciona intestinalis in mammalian cells and transgenic flies. In the fruit-fly, AOX expression overcomes the lethality of poisons directed at mitochondria, and cures flies of genetic defects that produce features equivalent to PD or fatal mitochondrial diseases of infancy. Preliminary data on mammalian models also indicates that the gene can be safely expressed, and contributes similar benefits. These now constitute a key validation tool to test the potential for AOX therapy of many human diseases. This PoC project will undertake the crucial next steps in the development of AOX therapy by implementing a partner search and negotiating terms for testing the technology in many different mammalian models of common diseases associated with mitochondrial dysfunction, and by soliciting major investment for the development of AOX therapy from both public and private-sector partners.'