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RoBE SIGNED

Study of the role of BANK1 in antibody production and antibody-independent functions of B cells in SLE

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 RoBE project word cloud

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

inflammatory    class    mice    protein    bank1    self    regulates    exert    antigens    tlr7    igg    cells    transcription    cell    atac    reported    total    chromatin    function    susceptible    cytometry    model    sequencing    switch    aberrant    antibodies    primarily    rna    differentiation    recombination    pathogenic    ankyrin    therapeutic    molecular    mechanisms    hypothesize    mediator    ed    igg2c    mass    drives    disease    cytokines    roles    pro    effector    examine    underlying    systemic    chip    generation    incurable    immunoprecipitation    circulating    exaggerated    absence    transposase    previously    acid    autoantibodies    accessible    sle    independent    life    pathogenesis    autoimmune    women    regulate    functions    flow    scaffold    plays    seq    identification    poorly    lupus    hyperactivation    nuclear    followed    mechanism    mouse    threatening    activation    data    understand    avenues    erythematosus    deep    suggest    cytokine    antibody    signaling    participation    assay   

Project "RoBE" data sheet

The following table provides information about the project.

Coordinator
FUNDACION PUBLICA ANDALUZA PROGRESO Y SALUD 

Organization address
address: AVENIDA AMERICO VESPUCIO 15 EDIF S2
city: SEVILLA
postcode: 41092
website: www.juntadeandalucia.es/fundacionprogresoysalud

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 259˙398 €
 EC max contribution 259˙398 € (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-CAR
 Starting year 2019
 Duration (year-month-day) from 2019-09-16   to  2022-10-21

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    FUNDACION PUBLICA ANDALUZA PROGRESO Y SALUD ES (SEVILLA) coordinator 259˙398.00

Map

 Project objective

Systemic Lupus Erythematosus (SLE, Lupus) is a life-threatening and incurable autoimmune disease that affects primarily women, its pathogenesis is related with an exaggerated B cells activation that results both in the generation of antibodies against self-nuclear acid antigens and in the generation of subsets of B cells that can exert antibody-independent roles in Lupus. However, the mechanisms that regulate aberrant B cell functions are poorly understood. In this project, we propose to investigate the role of the B cell scaffold protein with ankyrin repeats 1 (BANK1) in the B cell activation signaling pathways in a mouse model of Lupus. We have previously reported that the absence of BANK1 signaling in mice susceptible to Lupus resulted in the reduction of the activation of B cells, circulating total IgG2c and IgG autoantibodies, pro-inflammatory cytokines, and transcription factors related with TLR7 activation. Our data suggest that BANK1 is an important mediator of B cell hyperactivation. We hypothesize that BANK1 plays an important role in B cell signaling affecting their activation and effector functions in Lupus, however we do not fully understand yet the mechanism behind the function of BANK1. Our specific aims are: 1) to define how BANK1 signaling drives class switch recombination, 2) to determine the mechanism by which BANK1 regulates the cytokine production in B cells, and 3) to examine the participation of BANK1 signaling in the differentiation of pathogenic B cell subsets. To accomplish our objectives, we will use flow and mass cytometry, RNA-based next-generation sequencing (RNA-seq) analysis, the assay for transposase-accessible chromatin followed by deep sequencing (ATAC-seq), and a chromatin immunoprecipitation (ChIP) assay. We expect that the results of these studies will help to understand the molecular mechanism underlying the pathogenic B cell response in Lupus and will lead to identification of new avenues for therapeutic development.

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