DDRNA

A novel direct role of non coding RNA in DNA damage response activation

 Coordinatore IFOM FONDAZIONE ISTITUTO FIRC DI ONCOLOGIA MOLECOLARE 

Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.

 Nazionalità Coordinatore Italy [IT]
 Totale costo 2˙329˙200 €
 EC contributo 2˙329˙200 €
 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-2012-ADG_20120314
 Funding Scheme ERC-AG
 Anno di inizio 2013
 Periodo (anno-mese-giorno) 2013-06-01   -   2018-05-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    IFOM FONDAZIONE ISTITUTO FIRC DI ONCOLOGIA MOLECOLARE

 Organization address address: "Via Adamello, 16"
city: MILAN
postcode: 20139

contact info
Titolo: Dr.
Nome: Carlo
Cognome: Raimondi Cominesi
Email: send email
Telefono: +39 02 574303256
Fax: +39 02 574303231

IT (MILAN) hostInstitution 2˙329˙200.00
2    IFOM FONDAZIONE ISTITUTO FIRC DI ONCOLOGIA MOLECOLARE

 Organization address address: "Via Adamello, 16"
city: MILAN
postcode: 20139

contact info
Titolo: Dr.
Nome: Fabrizio
Cognome: D'adda Di Fagagna
Email: send email
Telefono: +39 02 574303227
Fax: +39 02 574303231

IT (MILAN) hostInstitution 2˙329˙200.00

Mappa


 Word cloud

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

damage    cells    evolutionary    conserved    repaired    ddr    we    dna    cell    species    rna    activation   

 Obiettivo del progetto (Objective)

'DNA, if damaged, cannot be replaced. If not replaceable, it must be repaired. The so-called “DNA damage response” (DDR) is a coordinate set of evolutionary conserved events that arrest the cell-cycle (DNA damage checkpoint function) in proliferating cells and attempts DNA repair. Until DNA damage has not been repaired in full, cell proliferation is not resumed in normal cells. DNA damage is a physiological event. Ageing and cancer are both associated with DNA damage accumulation. In the past, we contribute to better understand the mechanisms and the consequences of DNA damage generation and DDR activation in both settings.

We have recently identified a completely hitherto undiscovered level of control of DDR activation, so far considered a proteinaceous only signaling cascade. We have discovered that short RNA species are detectable at DNA damage sites and are necessary for DDR activation at DNA lesions. These RNA species are generated by an evolutionary-conserved RNA processing machinery. However, they serve purposes never reported before. We believe that our findings change radically our understanding of DDR modulation in mammals and disclose a fertile unspoilt ground for exciting investigations.'

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