T2DCREBBP

Defining the molecular basis of type 2 diabetes predisposition through targeted sequencing of the CREBBP-interacting gene network

Coordinatore	THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD    more  Organization address address: University Offices, Wellington Square city: OXFORD postcode: OX1 2JD contact info Titolo: Ms. Nome: Gill Cognome: Wells Email: send email Telefono: +44 1865 289800 Fax: +44 1865 289801
Nazionalità Coordinatore	United Kingdom [UK]
Totale costo	309˙235 €
EC contributo	309˙235 €
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-2012-IEF
Funding Scheme	MC-IEF
Anno di inizio	2013
Periodo (anno-mese-giorno)	2013-05-01   -   2015-04-30

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD  Organization address address: University Offices, Wellington Square city: OXFORD postcode: OX1 2JD contact info Titolo: Ms. Nome: Gill Cognome: Wells Email: send email Telefono: +44 1865 289800 Fax: +44 1865 289801	UK (OXFORD)	coordinator	309˙235.20

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 Obiettivo del progetto (Objective)

Type 2 diabetes (T2D) represents a major challenge to global health. In recent years, over 60 genetic loci have been confidently implicated in T2D predisposition: however, there has been only limited progress in defining the biological mechanisms responsible. Recent work led by the host institution has revealed that these T2D-associated loci are substantially enriched for genes whose protein products interact with CREBBP, identifying this transcriptional co-activator as a key node linking processes involved in T2D development. The research I propose to conduct aims to explore the overall contribution of the CREBBP interactome in T2D predisposition, through integration of existing and novel genetic data. The former is provided by extensive genome wide association (n~100,000 individuals), exome sequence (n~14,000) and exome chip (n~60,000) available to the host institution; the latter will be generated by the applicant through large-scale (>20,000 individuals), targeted resequencing of genes coding for key CREBBP-interacting proteins. Through these data, I expect to generate a comprehensive evaluation of the genetic evidence linking CREBBP-interacting proteins to T2D pathogenesis, laying the foundation for further functional studies. As well as the intrinsic scientific merit of this proposal, the research outlined will provide extensive training in state-of-the-art experimental and analytical methods in human genetics