DNCURE

Dynamic signalling networks in Diabetic Nephropathy (DN) – New avenues to a personalized therapy.-

Coordinatore	UNIVERSITAETSKLINIKUM FREIBURG    more Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.
Nazionalità Coordinatore	Germany [DE]
Totale costo	1˙999˙920 €
EC contributo	1˙999˙920 €
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-CoG
Funding Scheme	ERC-CG
Anno di inizio	2014
Periodo (anno-mese-giorno)	2014-06-01   -   2019-05-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	UNIVERSITAETSKLINIKUM FREIBURG  Organization address address: HUGSTETTER STRASSE 49 city: FREIBURG postcode: 79106 contact info Titolo: Mrs. Nome: Maren Cognome: Mihlan Email: send email Telefono: +49 761 27084420 Fax: +49 761 27018890	DE (FREIBURG)	hostInstitution	1˙999˙920.00
2	UNIVERSITAETSKLINIKUM FREIBURG  Organization address address: HUGSTETTER STRASSE 49 city: FREIBURG postcode: 79106 contact info Titolo: Prof. Nome: Tobias Georg Bruno Maria Cognome: Huber Email: send email Telefono: +49 761 27035590 Fax: +49 761 27032700	DE (FREIBURG)	hostInstitution	1˙999˙920.00

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 Obiettivo del progetto (Objective)

'Dynamic signalling networks in Diabetic Nephropathy (DN) – New avenues to a personalized therapy.- We have developed an exquisite experimental platform that facilitates the systematic unravelling of the signalling networks leading to (1) the initiation, (2) the progression and (3) the potential regeneration of podocytes in DN, paving the way to novel therapeutic strategies: (1) DN initiation: Identification of signalling cascades leading to microalbuminuria: Molecular By combining transgenic Drosophila lines carrying secreted fluorescent proteins to monitor the barrier function in vivo with a genome-wide siRNA screen we will establish a unique system to directly identify gene networks contributing to microalbuminuria. (2a) DN progression: Molecular fingerprinting of podocyte degeneration: Based on a transgenic fluorescent mouse model, we have pioneered a highly efficient podocyte purification method from type1 and type 2 diabetic mice allowing us to develop a precise molecular genetic, quantitative proteomic and micro RNA fingerprint from freshly isolated podocytes from diabetic and non-diabetic mice. (2b) DN progression: We established a proteomic approach to measure site-specific phosphorylation dynamics in primary podocyte cultures originating from transgenic mice that are TORC1 deficient, TORC2 deficient or TORC1 hyperactive (TSC1 KO) solely in the podocytes. (3) Potential role of podocyte regeneration in DN: Finally, to target mechanisms that could potentially reverse the disease process (by repopulating lost podocytes), we invented a strategy to quantitatively monitor podocyte turnover from different stem cell niches allowing us to precisely assess and potentially manipulating the capacity of podocyte regeneration in DN.'