Coordinatore | KRAEFTENS BEKAEMPELSE
Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie. |
Nazionalità Coordinatore | Denmark [DK] |
Totale costo | 2˙499˙960 € |
EC contributo | 2˙499˙960 € |
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-2013-ADG |
Funding Scheme | ERC-AG |
Anno di inizio | 2014 |
Periodo (anno-mese-giorno) | 2014-02-01 - 2019-01-31 |
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1 |
KRAEFTENS BEKAEMPELSE
Organization address
address: Strandboulevarden 49 contact info |
DK (KOEBENHAVN) | hostInstitution | 2˙499˙960.00 |
2 |
KRAEFTENS BEKAEMPELSE
Organization address
address: Strandboulevarden 49 contact info |
DK (KOEBENHAVN) | hostInstitution | 2˙499˙960.00 |
Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.
'Knowing that the lysosomes contain a powerful cocktail of hydrolases capable of digesting cells and entire tissues, it is obvious that the maintenance of lysosomal membrane integrity is of utmost importance for all cells, and especially for cancer cells with dramatically increased lysosomal activity. Yet, the mechanisms that regulate lysosomal membrane stability have remained obscure, largely due to the lack of methods sensitive enough to detect partial lysosomal leakage and suitable for screening purposes. We have finally succeeded in developing such a method, which allows me to propose here a project whose major aim is to reveal how cells maintain the integrity of lysosomal membranes. Based on our emerging data that firmly connect heat shock protein 70 and sphingolipid metabolism to lysosomal membrane stability, we will devote a large part of the project to the molecular details of these connections and to the characterization of the effects of new and already approved (cationic amphiphilic drugs) sphingolipid-regulating drugs on lysosomal membrane stability and cell survival. Additionally, we will screen selected siRNA libraries to identify signaling networks and lysosome-associated proteins essential for lysosomal membrane integrity, and small molecule libraries to identify compounds that induce lysosomal cell death. The next step is to identify lysosome-stabilizing mechanisms that are especially important for cancer cell survival. And the ultimate goal is to validate corresponding drug targets and drugs (old and new) for the induction of lysosomal cell death in therapy resistant cancers. As a “by-product” we expect to identify putative drug targets for the treatment of degenerative diseases and lipid storage disorders, where the stabilization of the lysosomal membranes promotes cell survival.'
Unraveling the molecular mechanisms leading to cellular dysfunction in diseases linked to defects in mitochondrial iron-sulfur cluster metabolism
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