ROS IN CELL FATE

Influence of oxidants on cell fate determination by use of a GFP coupled redox sensor

 Coordinatore DEUTSCHES KREBSFORSCHUNGSZENTRUM 

 Organization address address: Im Neuenheimer Feld 280
city: HEIDELBERG
postcode: 69120

contact info
Titolo: Ms.
Nome: Bettina
Cognome: Crispin
Email: send email
Telefono: -8914
Fax: -8922

 Nazionalità Coordinatore Germany [DE]
 Totale costo 158˙694 €
 EC contributo 158˙694 €
 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-2007-2-1-IEF
 Funding Scheme MC-IEF
 Anno di inizio 2009
 Periodo (anno-mese-giorno) 2009-12-01   -   2011-11-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    DEUTSCHES KREBSFORSCHUNGSZENTRUM

 Organization address address: Im Neuenheimer Feld 280
city: HEIDELBERG
postcode: 69120

contact info
Titolo: Ms.
Nome: Bettina
Cognome: Crispin
Email: send email
Telefono: -8914
Fax: -8922

DE (HEIDELBERG) coordinator 0.00

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 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

cell    cells    fibroblasts    levels    differentiation    culture    adult    ros    cellular    oxygen    senescence    intracellular    endogenous    redox    death   

 Obiettivo del progetto (Objective)

'Reactive oxygen species are derivatives of aerobic metabolism. Their production is finely regulated to protect cells against severe and permanent damage to cellular components that could ultimately lead to programmed cell death. However at low levels, ROS act as second messagers in several signalling pathways leading to growth, differentiation, senescence or cell death. This dual function of ROS appears to be due to differences in their concentrations, their sub-cellular localization and the pulse-duration. Using a newly developed fluorescent redox biosensor that allows dynamic live imaging of the intracellular glutathione redox state, I will study the role of endogenous oxidants in cell fate decision at the G1 checkpoint. I will follow the intracellular redox state of 3 primary cell types as they grow in culture, respond to mitogenic stimuli or differentiation factors and undergo senescence. Oxygen sensitivity of these processes will be also evaluated by modifying the oxygen culture conditions. Murine adult neural stem cells will serve as a model to study the balance between self-renewal and differentiation while mouse embryonic fibroblasts and human adult skin fibroblasts will be studied in terms of proliferative capacity versus senescence induction. Furthermore, we plan to generate transgenic mice constitutively expressing the redox sensor. This will allow us to compare endogenous redox levels in different tissues, over time and under pathological conditions.'

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