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Beta-splicenet

ALTERNATIVE SPLICING NETWORKS IN PANCREATIC BETA CELLS

Total Cost €

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EC-Contrib. €

0

Partnership

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 Beta-splicenet project word cloud

Explore the words cloud of the Beta-splicenet project. It provides you a very rough idea of what is the project "Beta-splicenet" about.

network    indicate    proteins    glis3    gt    epitopes    rbps    human    splice    mrna    alternative    bh3    combine    inflammation    generator    diversity    mechanism    inflammatory    extracellular    signals    bim    triggered    apoptosis    ultimate    provides    t1d    inference    proteome    protein    validate    suggest    90    candidate    death    activate    autoimmunity    discovered    plays    regulation    type    killed    rna    diabetes    infiltrating    cellular    molecules    cytokines    lost    pro    mechanisms    modify    exquisite    progressive    disease    biology    clarified    group    fate    transcriptome    genes    nature    aggravated    autoimmune    seq    modulation    therapeutic    nothing    released    diseases    functional    networks    beta    gene    individual    expression    strategy    decide    prevent    activated    cell    dysfunction    3000    binding    survival    intracellular    nearly    pancreatic    cues    splicing    host    immune    generation    antigenic    apoptotic    hypothesise    cells    regulating    potent    capacity    chronic    variants   

Project "Beta-splicenet" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITE LIBRE DE BRUXELLES 

Organization address
address: AVENUE FRANKLIN ROOSEVELT 50
city: BRUXELLES
postcode: 1050
website: www.ulb.ac.be

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 Belgium [BE]
 Project website http://www.ulb.ac.be/recherche/presentation/en-mariecurieprojetsen.html
 Total cost 160˙800 €
 EC max contribution 160˙800 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2014
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2015
 Duration (year-month-day) from 2015-06-01   to  2017-05-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITE LIBRE DE BRUXELLES BE (BRUXELLES) coordinator 160˙800.00

Map

 Project objective

Type 1 diabetes (T1D) is a chronic autoimmune disease in which pancreatic beta cells are killed by infiltrating immune cells and by cytokines released by these cells. The mechanisms by which autoimmunity is triggered and aggravated in T1D and the nature of the intracellular signals that decide beta cell fate between survival or death remain to be clarified. Alternative splicing (AS) is a complex mechanism of gene expression regulation and a potent generator of proteome diversity. It provides cells with an exquisite capacity to rapidly modify their transcriptome and proteome in response to intra and extracellular cues. AS affects more than 90% of human genes and has a major impact in many cellular processes, including cell survival and generation of new antigenic epitopes. There is a growing interest in the role of AS in autoimmune diseases but nearly nothing is known on its role in beta cells and diabetes. Recent findings by the host group indicate that pro-inflammatory cytokines change the expression of >30 RNA-binding proteins (RBPs) and modify AS of >3000 genes in human beta cells. Importantly, the host group has discovered that the diabetes candidate gene GLIS3 affects beta cell apoptosis by regulating the splicing of the pro-apoptotic BH3-only protein Bim. These findings suggest that AS plays an important role in the regulation of beta cell dysfunction and death by mechanisms that remain to be clarified. We hypothesise that pro-inflammatory signals activate splicing networks contributing to beta cell functional lost and death. We propose in the present project a systems biology approach that will combine RNA-seq, network inference and analysis of individual RBPs to characterize and validate inflammation-activated splicing networks in beta cells. The ultimate goal is to identify key splicing networks and mRNA splice variants that will be targeted by splicing-modulation molecules as a novel therapeutic strategy to prevent progressive beta cell loss in T1D.

 Publications

year authors and title journal last update
List of publications.
2017 Jonàs Juan-Mateu, Tatiana H. Rech, Olatz Villate, Esther Lizarraga-Mollinedo, Anna Wendt, Jean-Valery Turatsinze, Letícia A. Brondani, Tarlliza R. Nardelli, Tatiane C. Nogueira, Jonathan L. S. Esguerra, Maria Inês Alvelos, Piero Marchetti, Lena Eliasson, Décio L. Eizirik
Neuron-enriched RNA-binding Proteins Regulate Pancreatic Beta Cell Function and Survival
published pages: 3466-3480, ISSN: 0021-9258, DOI: 10.1074/jbc.M116.748335
Journal of Biological Chemistry 292/8 2019-07-24
2016 Fabio Arturo Grieco, Guido Sebastiani, Jonas Juan-Mateu, Olatz Villate, Laura Marroqui, Laurence Ladrière, Ksenya Tugay, Romano Regazzi, Marco Bugliani, Piero Marchetti, Francesco Dotta, Décio L. Eizirik
MicroRNAs miR-23a-3p, miR-23b-3p, and miR-149-5p Regulate the Expression of Proapoptotic BH3-Only Proteins DP5 and PUMA in Human Pancreatic β-Cells
published pages: 100-112, ISSN: 0012-1797, DOI: 10.2337/db16-0592
Diabetes 66/1 2019-07-24
2016 Jonàs Juan-Mateu, Olatz Villate, Décio L Eizirik
MECHANISMS IN ENDOCRINOLOGY: Alternative splicing: the new frontier in diabetes research
published pages: R225-R238, ISSN: 0804-4643, DOI: 10.1530/EJE-15-0916
European Journal of Endocrinology 174/5 2019-07-24

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

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