Coordinatore | THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE
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Nazionalità Coordinatore | United Kingdom [UK] |
Totale costo | 2˙482˙492 € |
EC contributo | 2˙482˙492 € |
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-2010-AdG_20100317 |
Funding Scheme | ERC-AG |
Anno di inizio | 2011 |
Periodo (anno-mese-giorno) | 2011-05-01 - 2016-04-30 |
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1 |
THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE
Organization address
address: The Old Schools, Trinity Lane contact info |
UK (CAMBRIDGE) | hostInstitution | 2˙482˙492.00 |
2 |
THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE
Organization address
address: The Old Schools, Trinity Lane contact info |
UK (CAMBRIDGE) | hostInstitution | 2˙482˙492.00 |
Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.
'The prime objective for every life form is to deliver its genetic material, intact, to the next generation. Each human cell receives tens-of-thousands of DNA lesions per day. These lesions can block genome replication and transcription, and if not repaired or repaired incorrectly, they lead to mutations or wider genome aberrations that threaten cell viability. To counter such threats, life has evolved the DNA-damage response (DDR), to detect DNA damage, signal its presence and mediate its repair. DDR events impact on many cellular processes and, crucially, prevent diverse human diseases that include cancer, neurodegenerative diseases, immune-deficiencies and premature ageing. While much progress has been made in identifying DDR proteins, much remains to be learned about the molecular and cellular functions that they control. Furthermore, the frequent reporting of new DDR proteins in the literature suggests that many others await identification. The main goals for the proposed research are to: identify important new DDR-proteins and DDR-modulators, particularly those responding to DNA double-strand breaks (DSBs); provide mechanistic insights into how these proteins function; and determine how DDR events are affected by chromatin structure, by molecular chaperones and components of the Ubiquitin and Sumo systems. To achieve these ends, we will use molecular biology, biochemical, cell-biology and molecular genetics approaches, including synthetic-lethal and phenotypic-suppression screening methods in human cells and in the nematode worm. This work will not only be of academic importance, but will also indicate how DDR dysfunction can cause human disease and how such diseases might be better diagnosed and treated.'