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STEMCELLGERONTOGENES

Longevity and aging associated genes that control self-renewal and function of adult stem cells during aging

Coordinatore	LEIBNIZ-INSTITUT FUR ALTERSFORSCHUNG - FRITZ-LIPMANN-INSTITUT E.V. Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.
Nazionalità Coordinatore	Germany [DE]
Totale costo	2˙498˙400 €
EC contributo	2˙498˙400 €
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-2012-ADG_20120314
Funding Scheme	ERC-AG
Anno di inizio	2013
Periodo (anno-mese-giorno)	2013-07-01 - 2018-06-30

Partecipanti

#	participant	country	role	EC contrib. [€]
1	LEIBNIZ-INSTITUT FUR ALTERSFORSCHUNG - FRITZ-LIPMANN-INSTITUT E.V. Organization address address: BEUTENBERGSTRASSE 11 city: JENA postcode: 7745 contact info Nome: Babette Cognome: Scherneck Email: send email Telefono: +49 3641 656237 Fax: +49 3641 656351	DE (JENA)	hostInstitution	2˙498˙400.00
2	LEIBNIZ-INSTITUT FUR ALTERSFORSCHUNG - FRITZ-LIPMANN-INSTITUT E.V. Organization address address: BEUTENBERGSTRASSE 11 city: JENA postcode: 7745 contact info Titolo: Prof. Nome: Karl Lenhard Cognome: Rudolph Email: send email Telefono: +49 3641 656334 Fax: +49 3641 656351	DE (JENA)	hostInstitution	2˙498˙400.00

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reverse aging longevity humans rnai indicate functional adult delineate experimental loci mammalian analyzing molecular genes cell vivo maintenance function mice data genetic regeneration stem organ mechanisms cells associations

Obiettivo del progetto (Objective)

'Adult stem cells are essential for the lifelong maintenance and regeneration of various organs and tissues. Experimental and clinical data indicate that the functional capacity of adult stem cells in organ regeneration declines during aging. Molecular mechanisms that cause impairments in stem cell function during aging remain to be delineated. Genetic analyses identified a growing number of genes and genetic loci that are associated with longevity and aging in model organisms and humans. For most of these associations the molecular mechanisms and its functional relevance for mammalian aging remain unknown. In many cases of genetic loci associations, the responsible genes have not even been identified. A bottleneck in our understanding of aging remains to identify functionally relevant genes and molecular mechanisms from this growing list of genetic association with aging. Emerging experimental data indicate that aging/longevity-associated genes influence the functional reserve of adult stem cells. Here, I propose to develop and lead a research program analyzing longevity and aging associated genes and gene loci by reverse genetic approaches. In vivo and ex vivo RNAi will identify genes and molecular mechanisms that affect the function of stem cells in aging mice or genetically engineered mice modeling accelerated accumulation of molecular damages and stem cell dysfunction. Analysis of primary human stem cells from young vs. old donors will delineate whether the identified genes and mechanisms are conserved in humans. Reverse genetic approaches of aging/longevity-associated genes have not been conducted in adult mammalian stem cells. Our group gained significant expertise in analyzing molecular mechanisms of stem cell maintenance and function as well as in conducting RNAi screens in different murine stem cell compartments. Our studies will delineate novel mechanisms of stem cell aging and its implication for defects in organ homeostasis and regeneration during aging.'