Opendata, web and dolomites

HUNTINFISH SIGNED

Generation of new zebrafish models for the study of the pathogenesis of Huntington´s disease and for the identification of new therapeutic targets.

Total Cost €

0

EC-Contrib. €

0

Partnership

0

Views

0

 HUNTINFISH project word cloud

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

organism    construct    date    human    lines    clearance    fluorescent    genome    inhibition    neuroinflammation    proteasome    examine    drugs    context    inflammasome    ubiquitin    autophagy    uas    toxic    host    treatments    glial    polyglutamine    trinucleotide    zebrafish    incurable    wild    proteins    model    neurodegenerative    exon1    autosomal    prevent    length    hd    cycles    expansions    tools    accelerate    polyq    protein    stimulation    misfolding    fish    cag    abnormally    gain    transgenic    previously    strategies    modeling    unfortunately    complicated    slow    photoconvertible    expressing    fused    kinetics    shared    diseases    lab    forms    straightforward    vivo    mutant    life    neurons    models    me    recapitulates    tissues    dendra    aggregation    deeper    first    nine    integration    huntingtin    gal4    huntington    tract    disorder    dominant    acute    tracts    played    disease    htt    encode    validate    relevance    mentioned    nd    advantage    full    body    therapies    vitro    caused    cells    therapeutic    generate    pathogenesis   

Project "HUNTINFISH" data sheet

The following table provides information about the project.

Coordinator
THE CHANCELLOR MASTERS AND SCHOLARSOF THE UNIVERSITY OF CAMBRIDGE 

Organization address
address: TRINITY LANE THE OLD SCHOOLS
city: CAMBRIDGE
postcode: CB2 1TN
website: www.cam.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 183˙454 €
 EC max contribution 183˙454 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2016
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2018
 Duration (year-month-day) from 2018-05-01   to  2020-04-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE CHANCELLOR MASTERS AND SCHOLARSOF THE UNIVERSITY OF CAMBRIDGE UK (CAMBRIDGE) coordinator 183˙454.00

Map

 Project objective

Huntington´s disease (HD) is one of the nine neurodegenerative diseases (ND) caused by (CAG)n trinucleotide tract expansions that encode abnormally long polyglutamine (polyQ) tracts. The common features shared by many ND are the misfolding and aggregation of toxic proteins. Thus, HD recapitulates features of other, more complicated ND. As HD is an autosomal dominant disorder, modeling this disease in vitro and in vivo is straightforward. Unfortunately, HD is, to date, incurable and there are no drugs or therapies that are known to slow or prevent the disease. Thus, the strategies proposed in this project, taking advantage of the unique characteristics of the zebrafish as model organism to study human diseases, will allow me to gain a deeper understanding of its pathogenesis, and to generate tools to accelerate the development of new therapies. Moreover, my findings may have relevance to other ND. First, I propose to generate new zebrafish transgenic lines expressing different forms of human huntingtin (htt) (wild-type/mutant, full-length/exon1) fused to the photoconvertible fluorescent protein Dendra in whole body, neurons or glial cells using the UAS-GAL4 system. Next, I will validate the construct integration in the fish genome and characterize the transgenic lines. After that, I will use these new generated models to study the life cycles of the previously mentioned forms of htt in vivo, and I will examine their clearance kinetics in vivo in different tissues in the context of inhibition/stimulation of autophagy or ubiquitin-proteasome pathways. Moreover, I will assess the role played by the inflammasome in the context of the neuroinflammation present in HD. Finally, I will use these new zebrafish lines to test novel therapeutic targets recently identified in the host lab, in order to develop new treatments for HD.

Are you the coordinator (or a participant) of this project? Plaese send me more information about the "HUNTINFISH" project.

For instance: the website url (it has not provided by EU-opendata yet), the logo, a more detailed description of the project (in plain text as a rtf file or a word file), some pictures (as picture files, not embedded into any word file), twitter account, linkedin page, etc.

Send me an  email (fabio@fabiodisconzi.com) and I put them in your project's page as son as possible.

Thanks. And then put a link of this page into your project's website.

The information about "HUNTINFISH" are provided by the European Opendata Portal: CORDIS opendata.

More projects from the same programme (H2020-EU.1.3.2.)

COLEX (2019)

Coopetition and Legislation in the Spanish Netherlands (1598-1665)

Read More  

NaWaTL (2020)

Narrative, Writing, and the Teotihuacan Language: Exploring Language History Through Phylogenetics, Epigraphy and Iconography

Read More  

GenEl (2020)

General readout electronics for cross-sectoral application in European research infrastructure

Read More