REMITODED

Regulating the Mitochondrial Decision to Die

Coordinatore	UNIVERSITY OF GLASGOW    more  Organization address address: University Avenue city: GLASGOW postcode: G12 8QQ contact info Titolo: Mr. Nome: Joe Cognome: Galloway Email: send email Telefono: +44 141 330 3884
Nazionalità Coordinatore	United Kingdom [UK]
Totale costo	100˙000 €
EC contributo	100˙000 €
Programma	FP7-PEOPLE Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	FP7-PEOPLE-2012-CIG
Funding Scheme	MC-CIG
Anno di inizio	2012
Periodo (anno-mese-giorno)	2012-12-01   -   2016-11-30

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	UNIVERSITY OF GLASGOW  Organization address address: University Avenue city: GLASGOW postcode: G12 8QQ contact info Titolo: Mr. Nome: Joe Cognome: Galloway Email: send email Telefono: +44 141 330 3884	UK (GLASGOW)	coordinator	100˙000.00

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 Obiettivo del progetto (Objective)

'The mitochondrial pathway of apoptosis is the major form of programmed cell death in vertebrates. In this pathway, pro-apoptotic members of the Bcl-2 protein family cause mitochondrial outer membrane permeabilisation (MOMP) leading to the release of mitochondrial intermembrane space proteins that activate caspase proteases and apoptosis. Regulation of MOMP has been intensively investigated because it represents a crucial, and potentially targetable, process that determines cell survival. Upon initiation, MOMP has previously been shown to occur synchronously and quickly in all mitochondria in less than ten minutes. However, using a new approach that mimics cancer cells that are primed to die, I find that the duration of MOMP can take over one hour in some cells (termed here slow MOMP). Importantly, cells that undergo slow MOMP fail to display overt signs of caspase activity and survive in the short-term, strongly indicating that caspase activity and kinetics of MOMP are tightly linked. My first objectives are to understand what controls differential MOMP kinetics and define how these regulate caspase activity and cell survival. Furthermore, I have recently found that some mitochondria can remain intact upon MOMP. This suggests that under normal or stressed conditions a minority of mitochondria can undergo MOMP without triggering apoptosis (termed here accidental MOMP). A second objective will be to investigate the occurrence of accidental MOMP and understand its impact upon caspase activity and cell viability. To meet both objectives I will use a variety of biochemical and cell biological methods including extensive and novel live-cell imaging techniques. This project will provide new insight into how MOMP and cell survival are regulated. It is expected that results and knowledge obtained from this work will contribute towards efforts to therapeutically target MOMP in various diseases such as cancer.'