HASKODIABETES

Adenosine receptors in diabetes

 Coordinatore INSTITUTE OF EXPERIMENTAL MEDICINE - HUNGARIAN ACADEMY OF SCIENCES 

 Organization address address: Szigony utca 43
city: Budapest
postcode: 1083

contact info
Titolo: Dr.
Nome: György
Cognome: Haskó
Email: send email
Telefono: (36)-1-2109400
Fax: (36)-1-2109423

 Nazionalità Coordinatore Hungary [HU]
 Totale costo 75˙000 €
 EC contributo 75˙000 €
 Programma FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call FP7-PEOPLE-2007-4-3-IRG
 Funding Scheme MC-IRG
 Anno di inizio 2008
 Periodo (anno-mese-giorno) 2008-04-01   -   2011-03-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    INSTITUTE OF EXPERIMENTAL MEDICINE - HUNGARIAN ACADEMY OF SCIENCES

 Organization address address: Szigony utca 43
city: Budapest
postcode: 1083

contact info
Titolo: Dr.
Nome: György
Cognome: Haskó
Email: send email
Telefono: (36)-1-2109400
Fax: (36)-1-2109423

HU (Budapest) coordinator 0.00

Mappa


 Word cloud

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receptor    adenosine    rejection    inflammatory    mice    graft    models    diabetes    receptors    immune    islet    diabetic   

 Obiettivo del progetto (Objective)

'Adenosine receptors are expressed on immune cells and other tissues thought to regulate inflammatory events in mammals. Adenosine receptors, when activated by endogenous ligands or exogenous analogs, may repress inflammatory and immune pathways that lead to the destruction of pancreatic islets in models of type I diabetes and islet graft rejection. Building on our observations that inosine and NECA, two adenosine receptor agonists, inhibit diabetes and islet graft rejection in non-obese diabetic mice and multiple-low-dose-streptozotocin-treated mice, we postulate that certain adenosine receptor subtypes play a protective role in these type 1 diabetic mouse models. There are four types of adenosine receptors, all of which are members of the G protein-coupled family of receptors. The genes for these receptors have been analyzed in detail and they are designated A1, A2A, A2B, and A3. In this proposal we will attempt to delineate the exact roles for the various adenosine receptors in modulating the development of diabetes. By identifying which receptor(s) mediate the adenosine-mediated suppression of diabetes, we can utilize this information to develop new therapeutic approaches that specifically target the receptor(s) of interest.'

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