CHRONEUROREPAIR

Chromatin states in neurogenesis – from understanding chromatin loops to eliciting neurogenesis for repair

 Coordinatore HELMHOLTZ ZENTRUM MUENCHEN DEUTSCHES FORSCHUNGSZENTRUM FUER GESUNDHEIT UND UMWELT GMBH 

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 Nazionalità Coordinatore Germany [DE]
 Totale costo 2˙376˙560 €
 EC contributo 2˙376˙560 €
 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-2013-ADG
 Funding Scheme ERC-AG
 Anno di inizio 2014
 Periodo (anno-mese-giorno) 2014-02-01   -   2019-01-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    HELMHOLTZ ZENTRUM MUENCHEN DEUTSCHES FORSCHUNGSZENTRUM FUER GESUNDHEIT UND UMWELT GMBH

 Organization address address: Ingolstaedter Landstrasse 1
city: MUENCHEN
postcode: 85764

contact info
Titolo: Dr.
Nome: Jürgen
Cognome: Ertel
Email: send email
Telefono: +49 89 3187 3022
Fax: +49 89 3187 3866

DE (MUENCHEN) hostInstitution 2˙376˙560.00
2    HELMHOLTZ ZENTRUM MUENCHEN DEUTSCHES FORSCHUNGSZENTRUM FUER GESUNDHEIT UND UMWELT GMBH

 Organization address address: Ingolstaedter Landstrasse 1
city: MUENCHEN
postcode: 85764

contact info
Titolo: Prof.
Nome: Magdalena
Cognome: Götz
Email: send email
Telefono: +49 89 31873750
Fax: +49 89 31873761

DE (MUENCHEN) hostInstitution 2˙376˙560.00

Mappa


 Word cloud

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transcriptional    neural    reprogramming    injury    vitro    neurogenic    fate    vivo    patient    conformation    neurogenesis    transcription    glial    trnp    brain    cell    chromatin    stem    aim    roles    molecular    cells    neuronal    regulation    mechanisms   

 Obiettivo del progetto (Objective)

'The mechanisms regulating neural stem cells and their progression to neurogenesis are important not only to understand brain development and evolution, but also to elicit neurogenesis after brain injury. Our recent findings imply novel chromatin-associated proteins in the regulation of neural stem cell fate and neurogenesis. Therefore this project aims to understand the molecular mechanisms of how these factors regulate neurogenesis in developing and adult mice (Aim1) and implement this knowledge for reprogramming glia into neurons after brain injury (Aim2). This will be pursued in mouse models in vivo (2.1) and with human glial cells derived from patient brain resections in vitro (2.2). It is well known that transcription factors need to alter the chromatin structure to achieve transcriptional regulation, but the factors involved in this regulation in neural stem and progenitor cells are still ill understood. Therefore the molecular function of the novel chromatin interacting protein Trnp1 with essential roles in neural stem cell (NSC) fate and the chromatin conformation mediated at neurogenic target genes by Pax6/Brg1-containing BAF complexes will be addressed in Aim1. Combined with genome-wide approaches to determine changes in chromatin conformation at neurogenic target gene sites this will greatly further our understanding of key roles of chromatin conformation in neural stem cells and neurogenesis. In Aim2 Trnp1 promoting neural stem cells fate and later acting neurogenic transcription factors will be used to improve neuronal reprogramming after stab wound injury in the murine brain in vivo and in patient-derived glial cells in vitro. Together with novel strategies to induce chromatin looping in a sequence-specific manner this project will not only advance our knowledge at the frontier of transcriptional regulation in neurogenesis, but also implement highly innovative approaches to utilize this knowledge for neuronal repair by direct reprogramming.'

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