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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.

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

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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