Explore the words cloud of the Beta-splicenet project. It provides you a very rough idea of what is the project "Beta-splicenet" about.
The following table provides information about the project.
UNIVERSITE LIBRE DE BRUXELLES
|Coordinator Country||Belgium [BE]|
|Total cost||160˙800 €|
|EC max contribution||160˙800 € (100%)|
1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
|Duration (year-month-day)||from 2015-06-01 to 2017-05-31|
Take a look of project's partnership.
|1||UNIVERSITE LIBRE DE BRUXELLES||BE (BRUXELLES)||coordinator||160˙800.00|
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.
|year||authors and title||journal||last update|
JonÃ s Juan-Mateu, Tatiana H. Rech, Olatz Villate, Esther Lizarraga-Mollinedo, Anna Wendt, Jean-Valery Turatsinze, LetÃcia A. Brondani, Tarlliza R. Nardelli, Tatiane C. Nogueira, Jonathan L. S. Esguerra, Maria InÃªs Alvelos, Piero Marchetti, Lena Eliasson, DÃ©cio 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|
Fabio Arturo Grieco, Guido Sebastiani, Jonas Juan-Mateu, Olatz Villate, Laura Marroqui, Laurence LadriÃ¨re, Ksenya Tugay, Romano Regazzi, Marco Bugliani, Piero Marchetti, Francesco Dotta, DÃ©cio 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 Î²-Cells
published pages: 100-112, ISSN: 0012-1797, DOI: 10.2337/db16-0592
JonÃ s Juan-Mateu, Olatz Villate, DÃ©cio 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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