PEROXIREDOXIN-CLOCK

A new intracellular metabolic timer mechanism to induce cell death selectively in cancer cells

 Coordinatore THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE 

 Organization address address: The Old Schools, Trinity Lane
city: CAMBRIDGE
postcode: CB2 1TN

contact info
Titolo: Ms.
Nome: Renata
Cognome: Schaeffer
Email: send email
Telefono: +44 1223 333543
Fax: +44 1223 332988

 Nazionalità Coordinatore United Kingdom [UK]
 Totale costo 231˙283 €
 EC contributo 231˙283 €
 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-2013-IEF
 Funding Scheme MC-IEF
 Anno di inizio 2014
 Periodo (anno-mese-giorno) 2014-08-04   -   2016-08-03

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE

 Organization address address: The Old Schools, Trinity Lane
city: CAMBRIDGE
postcode: CB2 1TN

contact info
Titolo: Ms.
Nome: Renata
Cognome: Schaeffer
Email: send email
Telefono: +44 1223 333543
Fax: +44 1223 332988

UK (CAMBRIDGE) coordinator 231˙283.20

Mappa


 Word cloud

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fellow    thinking    cell    biology    prx    apoptosis    cancer    progression    cells    host    cycle    cambridge    signaling    ros    regulated    he   

 Obiettivo del progetto (Objective)

'Peroxiredoxins (PRX) are at the heart of mechanisms gating the spatiotemporal distribution of ROS molecules within the cell and thereby deeply involved in the development or progression of disease. With the host group’s recent discovery on the circadian nature of PRX-hyperoxidation cycles, PRXs emerge to be tested for driving the physiological 24 h periodic fluctuations of the cellular redox state and ROS-signaling, both being critical in cell cycle control. The potential of the PRX-clock to robustly orchestrate cell cycle progression or apoptotic pathways will be analyzed in the proposed multidisciplinary study. The working hypothesis of the project is that this new timing mechanism operates even in rapidly proliferating cells and that it can be manipulated to deteriorate cancer cell survival selectively. Identification of new ROS-regulated targets promoting apoptosis specifically in transformed cells will have a huge impact on cancer therapy. At the host Institute in Cambridge, U.K., the Fellow will reveal post-transcriptionally regulated targets of PRX and their involvement in ROS-signaling and apoptosis induction in cancer. Through this project he will be able to address hot scientific issues and do important science in the future; furthermore, he will learn many new creative ways of thinking applied by world-renowned researchers in Cambridge. Know-how acquired during this training will open new intersectoral dimensions (Cell cycle biology, ROS biology) for the Fellow, and the evaluation of data obtained during the project will strengthen his interdisciplinary way of thinking.'

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