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B-different SIGNED

The RNA-Binding Protein ZFP36L1 regulates the terminal differentiation of B lymphocytes

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 B-different project word cloud

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

rna    remodelling    undergo    inhibits    immunoglobulin    implications    highest    immunity    secreting    function    binding    mouse    independent    employed    rbp    microenvironment    terminal    zfp36l1    reaction    rapid    regulation    lymphocyte    interplay    regulator    pc    scientist    expression    vaccines    me    reveal    antigen    governed    data    unknown    cells    indicating    commit    turn    transcriptional    decisions    unpublished    interactions    largely    technologies    managerial    transcriptome    multidisciplinary    acquire    levels    gene    germinal    biochemical    gcs    lymphomas    affinity    stringent    dysfunctional    expand    downstream    antibodies    uniquely    transduction    strength    skills    proteome    pioneers    bioinformatics    proteins    models    defective    expressing    dynamics    decision    cell    dictates    post    centre    plasma    gc    autoimmunity    fate    differentiation    edge    maturation    signal    elucidate    vitro    guarantees    expertise    career    mainly    unexplored    lab    cutting    humoral    host   

Project "B-different" data sheet

The following table provides information about the project.

Coordinator
THE BABRAHAM INSTITUTE 

Organization address
address: Babraham Hall
city: CAMBRIDGE
postcode: CB22 3AT
website: www.babraham.ac.uk

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 United Kingdom [UK]
 Total cost 212˙933 €
 EC max contribution 212˙933 € (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 2020-09-01   to  2022-08-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE BABRAHAM INSTITUTE UK (CAMBRIDGE) coordinator 212˙933.00

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 Project objective

Plasma cells (PC) secreting high-affinity antibodies are key for long-term immunity and the success of vaccines. PC are mainly generated within the germinal centre (GC), a microenvironment where B cells undergo affinity maturation and selection. The GC reaction guarantees that only B cells expressing immunoglobulin with the highest affinity for the antigen will commit to terminal differentiation. Stringent regulation is essential, as dysfunctional GC B cells can cause defective immunity, autoimmunity, or B-cell lymphomas. Affinity maturation requires rapid changes in the B cell transcriptome and proteome to enable cell fate decisions. This is governed by the interplay of signal transduction pathways and regulation at transcriptional and post-transcriptional levels. Post-transcriptional control is key for rapid remodelling of gene expression, yet its role in terminal differentiation remains largely unexplored. The host lab pioneers the study of RNA-binding proteins (RBP) in lymphocyte development and has unpublished data indicating that the RBP ZFP36L1 inhibits terminal differentiation of B cells in vitro. The regulation and function of ZFP36L1 in GCs is however unknown. In this proposal I will build on the unique and multidisciplinary expertise of the host lab and my experience on post-transcriptional regulation and immunity to address how ZFP36L1 dictates fate decision of B cells. Uniquely available mouse models will allow me to study how signal strength and signal transduction control ZFP36L1 activity and its downstream implications for humoral immunity. Cutting-edge technologies will be employed to elucidate the dynamics of ZFP36L1-RNA interactions and how they in turn define the proteome and fate of GC B cells. This work will reveal the role of an important new regulator of PC differentiation, and will enable me to expand my knowledge, acquire new biochemical, bioinformatics and managerial skills, and facilitate my career development as an independent scientist.

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