STEMRENEWAL

Identification of a new mechanism of stem cell self-renewal; direct implications on self-repair and tumor initiating cells in the brain

 Coordinatore KAROLINSKA INSTITUTET 

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 Nazionalità Coordinatore Sweden [SE]
 Totale costo 2˙492˙593 €
 EC contributo 2˙492˙593 €
 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-2008-AdG
 Funding Scheme ERC-AG
 Anno di inizio 2009
 Periodo (anno-mese-giorno) 2009-03-01   -   2014-02-28

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    KAROLINSKA INSTITUTET

 Organization address address: Nobels Vag 5
city: STOCKHOLM
postcode: 17177

contact info
Titolo: Ms.
Nome: Jill
Cognome: Blomstrand
Email: send email
Telefono: 46852487687
Fax: 468304452

SE (STOCKHOLM) hostInstitution 2˙492˙593.00
2    KAROLINSKA INSTITUTET

 Organization address address: Nobels Vag 5
city: STOCKHOLM
postcode: 17177

contact info
Titolo: Prof.
Nome: Patrik
Cognome: Ernfors
Email: send email
Telefono: 46852487659
Fax: 468341960

SE (STOCKHOLM) hostInstitution 2˙492˙593.00

Mappa


 Word cloud

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ligand    mechanisms    involving    stem    self    activation    pluripotency    niches    regulated    physiological    cells    normal    cell    unknown    proliferation    damage    mechanism    cycle    brain    nature    pathway    ddr   

 Obiettivo del progetto (Objective)

'The self-renewing nature of stem cells is a consequence of their ability to proliferate indefinitely while maintaining pluripotency. Mechanisms of pluripotency are well known but mechanisms controlling stem cell proliferation are unknown. Proliferation of somatic cells takes place in G1 cell cycle phase. We have identified that embryonic and peripheral neural stem cell proliferation is regulated by an entirely new mechanism involving chromatin remodeling and operating in the S/G2 phase of the cell cycle (Andang et al., Nature 2009). This involves the DNA damage response (DDR) pathway proteins. The DDR pathway is activated physiologically by GABA acting by the GABAA receptor leading to Cl- influx, cell swelling, and by unknown mechanism, activation of the PI3K related kinases ATR/ATM which phosphorylates histone H2AX. Combined, the data suggests that the DDR pathway is operating in a ligand-dependent manner under normal physiological conditions and that it may serve as a new molecular mechanism regulating cell proliferation in eukaryotic cells. We propose a homeostatic mechanism of stem cell proliferation where negative feedback control of the cell cycle adjusts stem cell numbers. The demonstration of normal, physiological, ligand-induced activation of these pathways in stem cell niches opens fundamentally new insight into the mechanisms of stem cell proliferation and surveillance against cancer. Once characterized, we propose that these mechanisms may be exploited to induce self repair following brain damage and to manipulate cell survival in tumor initiating cells of the brain (that share many characteristics with stem cells). The potential benefit of this proposed research could be vast, involving potentially a unifying mechanism how all stem cell niches in the embryo and in the adult individual is regulated and can be manipulated.'

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