TRANSPOSOSTRESS

Impact of stress-induced transposon activities on human disease

 Coordinatore MAX-DELBRUCK-CENTRUM FUR MOLEKULARE MEDIZIN IN DER HELMHOLTZ-GEMEINSCHAFT 

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 Nazionalità Coordinatore Germany [DE]
 Totale costo 1˙940˙725 €
 EC contributo 1˙940˙725 €
 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-2011-ADG_20110310
 Funding Scheme ERC-AG
 Anno di inizio 2013
 Periodo (anno-mese-giorno) 2013-01-01   -   2017-12-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    MAX-DELBRUCK-CENTRUM FUR MOLEKULARE MEDIZIN IN DER HELMHOLTZ-GEMEINSCHAFT

 Organization address address: ROBERT ROSSLE STRASSE 10
city: BERLIN
postcode: 13125

contact info
Titolo: Dr.
Nome: Ioannis
Cognome: Legouras
Email: send email
Telefono: +49 3094064247

DE (BERLIN) hostInstitution 1˙940˙725.00
2    MAX-DELBRUCK-CENTRUM FUR MOLEKULARE MEDIZIN IN DER HELMHOLTZ-GEMEINSCHAFT

 Organization address address: ROBERT ROSSLE STRASSE 10
city: BERLIN
postcode: 13125

contact info
Titolo: Prof.
Nome: Zsuzsanna
Cognome: Izsvák
Email: send email
Telefono: 493094000000

DE (BERLIN) hostInstitution 1˙940˙725.00

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 Word cloud

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transposon    genetic    sb    sequences    epigenetic    tes    induced    decipher    stress    genome    vector    mechanisms    model    human    disease    activation    te    first    impact    cancer   

 Obiettivo del progetto (Objective)

'The evolutionary success of transposable elements (TEs) is underscored by the finding that about 45% of the human genome is TE-derived. However, recent high throughput approach studies indicate that the impact of TE-associated activities was seriously underestimated. The first objective is to investigate the impact of TE-derived activities on the human genome in general and on disease mechanisms in particular, based on the central premise that some of these activities are stress-induced. To model how a vertebrate-specific transposon responds to stress signals in human cells, I will study molecular interactions of the Sleeping Beauty (SB) transposon with host cellular mechanisms to understand how stress-signalling and response triggers transposon activation. My second aim is to decipher the relationship between stress-induced activation of endogenous TEs and TE-derived regulatory sequences and human disease. I aim at investigating conditions and the consequences of activation of a particular copy of the MERmaid transposon located in the Sin3B transcriptional corepressor, frequently observed in cancer. The impact of global epigenetic remodelling will be investigated in the model of a complete (induced pluripotency) and partial (trans-differentiation) epigenetic reprogramming. In parallel, I aim at translating experience accumulated in TE research to cutting-edge technologies. First, the SB transposon will be adopted as a safe, therapeutic vector to treat age-dependent blindness (AMD). Second, a mutagenic SB vector will be used in a forward genetic screen to decipher a genetic network that protects against hormone-induced mammary cancer. The anticipated output of my research programme is a refined understanding of the consequences of environmental stress on our genome mediated by TE-derived sequences. The project is expected to provide an effective bridge between basic research and clinical- as well as technological translation of a novel gene transfer technology.'

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