Opendata, web and dolomites

transLEISHion SIGNED

A targeted knockout screen for identification of Leishmania membrane transporters required for infection of macrophages

Total Cost €

0

EC-Contrib. €

0

Partnership

0

Views

0

 transLEISHion project word cloud

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

proteins    form    fly    roles    infection    biology    thanks    molecular    causative    kinetoplastida    rapid    safer    hundreds    mechanisms    cheaper    hitherto    crispr    manipulation    unexplored    bite    viability    urging    transporters    sand    drug    allowed    amastigote    largely    leishmania    intrinsic    expressed    cellular    membrane    disease    proliferates    it    nutrient    leishmaniases    forms    survival    overexpressed    world    macrophages    functional    host    cas9    systematic    formulations    first    editing    acute    subvert    drawbacks    anti    gene    proposes    unclear    mutants    parasite    leishmanias    knockout    modern    phagolysosome    attack    agent    intracellular    transcriptomic    time    genes    promastigote    throughput    defence    genome    upregulated    interactions    extensively    functions    drugs    library    treatment    diseases    mediated    uncharacterized    pathogen    despite    generation    parasitic    cell    immune    48    amastigotes    transmitted    differentiation    mexicana    peptidases    harsh    identification    surface    encoding    macrophage    efforts   

Project "transLEISHion" data sheet

The following table provides information about the project.

Coordinator
THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD 

Organization address
address: WELLINGTON SQUARE UNIVERSITY OFFICES
city: OXFORD
postcode: OX1 2JD
website: www.ox.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 195˙454 €
 EC max contribution 195˙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-2017
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2018
 Duration (year-month-day) from 2018-09-01   to  2020-08-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD UK (OXFORD) coordinator 195˙454.00

Map

 Project objective

Leishmaniases are among the world's most neglected diseases. It´s causative agent - Leishmania - is transmitted by the bite of a sand fly. In the host, the parasite is taken up by macrophages and proliferates in the harsh conditions of the host phagolysosome. Currently available drugs for treatment present major drawbacks, urging the need for more effective, safer, and cheaper drugs. The molecular and cellular mechanisms that enable Leishmania to subvert macrophage defence mechanisms and cause disease remain largely unclear. Thanks to modern comparative transcriptomic analysis, the identification of hundreds of genes overexpressed in intracellular amastigote forms was possible for the first time and identified cell surface proteins, transporters, peptidases and many uncharacterized genes with possible roles in host-pathogen interactions. Only recently, a high-throughput gene editing method based on CRISPR-Cas9 allowed for the first time easy manipulation of Leishmanias´ complex genome and rapid functional analysis of genes. For over 50 years membrane transporters have been extensively studied in kinetoplastida, due to their role in the intrinsic parasite nutrient needs, defence from host immune attack and uptake of drug formulations. Despite these efforts a large number of such transporters expressed in amastigotes remain uncharacterized. The present project proposes (1) the generation of a library of 48 L. mexicana mutants by systematic CRISPR-Cas9 mediated knockout of amastigote-upregulated genes encoding membrane transporters, (2) Identification of membrane transporters required for viability of the promastigote parasite form and the (3) Identification of membrane transporters required for differentiation into amastigotes, macrophage infection, intracellular survival. The results of this project are expected to provide new insight into functions of hitherto unexplored aspects of amastigote biology and identify potential new targets for anti-parasitic drugs.

Are you the coordinator (or a participant) of this project? Plaese send me more information about the "TRANSLEISHION" 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 "TRANSLEISHION" are provided by the European Opendata Portal: CORDIS opendata.

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

MITafterVIT (2020)

Unravelling maintenance mechanisms of immune tolerance after termination of venom immunotherapy by means of clonal mast cell diseases

Read More  

NeuroTick (2019)

The neuroscience of tickling: cerebellar mechanisms and sensory prediction

Read More  

ReproMech (2019)

The Molecular Mechanisms of Cell Fate Reprogramming in Vertebrate Eggs

Read More