MIRNABETAIDENTITY

microRNAs confer robustness to adult beta–cell identity

 Coordinatore WEIZMANN INSTITUTE OF SCIENCE 

Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.

 Nazionalità Coordinatore Israel [IL]
 Totale costo 2˙000˙000 €
 EC contributo 2˙000˙000 €
 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) 2014-04-01   -   2019-03-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    WEIZMANN INSTITUTE OF SCIENCE

 Organization address address: HERZL STREET 234
city: REHOVOT
postcode: 7610001

contact info
Titolo: Dr.
Nome: Eran
Cognome: Hornstein
Email: send email
Telefono: +972 8 934 6215
Fax: +972 8 934 4108

IL (REHOVOT) hostInstitution 2˙000˙000.00
2    WEIZMANN INSTITUTE OF SCIENCE

 Organization address address: HERZL STREET 234
city: REHOVOT
postcode: 7610001

contact info
Titolo: Ms.
Nome: Gabi
Cognome: Bernstein
Email: send email
Telefono: +972 8 934 6728
Fax: +972 8 934 4165

IL (REHOVOT) hostInstitution 2˙000˙000.00

Mappa


 Word cloud

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

cell    our    de    differentiated    maintenance    genes    discoveries    cells    microrna    micrornas    adult    networks    beta    mechanisms    robustness    differentiation    identity   

 Obiettivo del progetto (Objective)

'Normal physiology depends on defined functional output of differentiated cells. A century of Developmental–Biology studies revealed diverse mechanisms for differentiation, however once ‘terminally’ differentiated, cells are thought to naïvely stay put. However differentiated cells are surprisingly fragile, for example, phenotypic collapse and de–differentiation of β–cells was recently discovered in pathogenesis of type 2 diabetes. These discoveries necessitate investigations of key questions: How is cell–type identity robustly maintained for decades in the adult organism? What are the genetic mechanisms for continuous maintenance of differentiation and identity? microRNAs, are known to impart robustness to differentiation. Do they play important roles in maintenance of adult β–cell identity?

Our overarching objective is to explore the exciting hypotheses that (i) Networks of microRNA and protein–coding genes are required to maintain adult cell identity. (ii) microRNAs confer robustness to adult β–cell identity by repressing disallowed genes that are deleterious to β–cells. (iii) Dysregulated microRNA disrupt cell identity and is a likely vector of pathology.

Our planned research has the potential of producing conceptual breakthroughs including: (1) Revolutionary view of microRNAs as agents of adult cell identity and discoveries of specific microRNAs that are crucial for maintaining β–cell identity (2) Experimental discovery of targets and networks involved in adult β–cell de-differentiation. (3) In–vivo evidence for combinatorial action of multiple microRNAs in control of β–cell identity. (4) Uncovering new links from de–differentiation and into metabolic diseases that may drive future medical innovation through usage of small RNAs to reinforce β–cell differentiation.'

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