HEPATOPANCREATIC

MECHANISMS UNDERLYING CELL FATE DECISION BETWEEN PANCREAS AND LIVER

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

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 Nazionalità Coordinatore Germany [DE]
 Totale costo 1˙186˙745 €
 EC contributo 1˙186˙745 €
 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-2009-StG
 Funding Scheme ERC-SG
 Anno di inizio 2009
 Periodo (anno-mese-giorno) 2009-11-01   -   2014-10-31

 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: Francesca M
Cognome: Spagnoli
Email: send email
Telefono: -94062534
Fax: -94062091

DE (BERLIN) hostInstitution 1˙186˙746.00
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: Dr.
Nome: Ioannis
Cognome: Legouras
Email: send email
Telefono: +49 3094064247
Fax: +49 3094062700

DE (BERLIN) hostInstitution 1˙186˙746.00

Mappa


 Word cloud

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

bipotent    cell    decision    disease    versus    arise    developmental    fate    diabetes    cells    sup    liver    regulators    mouse    adult    hepatic    pancreas    intrinsic    progenitor    pancreatic    lineage    reprogramming   

 Obiettivo del progetto (Objective)

'Diabetes is a degenerative disease affecting millions of persons worldwide. A cure for diabetes depends on replacing the insulin-producing ²-cells in the pancreas that are destroyed by the disease. An attractive strategy to attain this goal is to convert liver adult cells of the same patient into pancreatic ²-cells. The liver and pancreas share many aspects of their early development and are specified in adjacent regions of the endoderm, possibly from a common bipotent progenitor cell. Therefore, conversion of liver to pancreas is conceivable and should imply only few steps backward to a common progenitor and little epigenetic changes. However, how pancreatic versus hepatic fate decision occurs during development is still poorly understood. The aim of this proposal is two fold: to perform lineage analysis, and to study developmental regulators of pancreatic versus hepatic fate decision. We will use new genetic tools, based on the GFP and photoconvertible Kaede fluorescent proteins, to address: i. if the liver and pancreas arise from a common bipotent progenitor cell; ii. to trace in vivo; and iii. molecularly profile the presumptive precursor cell and its descendants in the mouse embryo. Our previous studies have identified target genes of the GATA factors that might act as intrinsic developmental regulators of the pancreatic versus hepatic fate decision. Both intrinsic factors together with extrinsic regulators, such as BMP, will be studied. We will test their potential to promote lineage reprogramming of liver to pancreas using the mouse as well as mouse embryonic stem cells as model systems. Understanding how distinct cell types arise from common multipotent progenitor cells is a major quest in developmental biology. Our findings will elucidate the spatiotemporal mechanisms that control pancreas versus liver fate decision. In addition, they will provide the blueprint for lineage reprogramming of adult hepatic cells to pancreas in diabetes cell-therapy.'

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