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ePANC-SPLICE SIGNED

Regulation and Function of Endocrine-Specific Splicing Programs in Pancreas and their Role in Diabetes

Total Cost €

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EC-Contrib. €

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Partnership

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Project "ePANC-SPLICE" data sheet

The following table provides information about the project.

Coordinator
FUNDACIO CENTRE DE REGULACIO GENOMICA 

Organization address
address: CARRER DOCTOR AIGUADER 88
city: BARCELONA
postcode: 8003
website: www.crg.es

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Spain [ES]
 Total cost 172˙932 €
 EC max contribution 172˙932 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2018
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2020
 Duration (year-month-day) from 2020-01-01   to  2021-12-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    FUNDACIO CENTRE DE REGULACIO GENOMICA ES (BARCELONA) coordinator 172˙932.00

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 Project objective

Pancreatic beta cells are highly specialized cells that play a key role in maintaining glucose homeostasis by secreting insulin. Dysfunction or loss of beta cells results in diabetes, a worldwide growing epidemic. Extensive research has started to uncover the signals and transcriptional networks that control specification, differentiation and maturity of the different pancreatic cell lineages, and in particular of beta cells. However, posttranscriptional regulation during pancreas development has remained mostly unexplored. Alternative splicing (AS) is the main posttranscriptional mechanism that generates transcriptomic and proteomic diversity, playing essential roles in cell specification and functional specialization. My previous data suggest that beta cells activate neuron-related splicing programs involved in the regulation of insulin secretion. Moreover, pro-inflammatory cytokines (mediators of beta cell failure in type 1 diabetes) affect the splicing of signaling and pro-apoptotic genes that determine beta cell survival. However, the presence of beta- or endocrine-specific splicing programs and their role in diabetes remains to be clarified. In this project, we will investigate the regulation and function of endocrine-specific alternative exons. I will combine comparative transcriptomics, biochemical and functional studies, iPCS reprogramming and zebrafish knock-outs to: (i) comprehensively identify endocrine-AS exons, and study their regulation during beta cell differentiation and pancreas development; (ii) probe the phenotypic impact of endocrine-AS programs on beta cell differentiation and function; and (iii) Investigate the role of ENDO-AS exons in remodeling transcriptional and signaling networks involved in diabetes. We foresee that this project will provide new insights into beta cell pathophysiology and generate valuable knowledge for the development of splicing-modulating therapies and disease biomarkers.

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The information about "EPANC-SPLICE" are provided by the European Opendata Portal: CORDIS opendata.

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