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QuinADAR1 SIGNED

Protection from malaria in the Fulani ethnic group of West Africa involves reduced levels of A-to-I RNA editing by ADAR1

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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Project "QuinADAR1" data sheet

The following table provides information about the project.

Coordinator
Masarykova univerzita 

Organization address
address: Zerotinovo namesti 9
city: BRNO STRED
postcode: 60177
website: http://www.muni.cz

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 Czech Republic [CZ]
 Total cost 144˙980 €
 EC max contribution 144˙980 € (100%)
 Programme 1. H2020-EU.4. (SPREADING EXCELLENCE AND WIDENING PARTICIPATION)
 Code Call H2020-WF-01-2018
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2019
 Duration (year-month-day) from 2019-06-01   to  2021-05-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    Masarykova univerzita CZ (BRNO STRED) coordinator 144˙980.00

Map

 Project objective

I will investigate what mediates an effective human immune response to infection with Plasmodium falciparum malaria.

I will approach this through studying the Fulani ethnic group of West Africa, who are relatively resistant to malaria infection. The basis of the Fulani protection from malaria has never been established. However, we have performed a pilot study which suggests that reduced levels of adenosine-to-inosine (A-to-I) editing of RNA by ADAR1 following P. falciparum infection can drive a more effective innate immune response in the Fulani.

We have an established collaboration with the Malaria Research and Training Centre at University of Sciences Technique and Technology in Mali, who have strong ties to the Fulani community. At Stockholm University, I have had the opportunity to develop a strong background in immunology research techniques, specifically utilizing in vitro models of malaria infection in human monocytes, in the research group of Eva Sverremark-Ekström. As the role of RNA modifications is an emerging field, I plan to move to CEITEC, Czech Republic, to work with Mary O’Connell, who has pioneered the role of A-to-I RNA modification in the innate immune response to RNA.

Specifically, we will test the hypothesis that reduced rates of A-to-I editing of RNA in the Fulani following infection enables them to mount a more effective innate immune response to P. falciparum malaria, and contributes to their relative protection from the disease. Further, targeting of ADAR1 and/or reduction in levels of A-to-I RNA levels may present a novel strategy to boost effective immune response to malaria.

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The information about "QUINADAR1" are provided by the European Opendata Portal: CORDIS opendata.

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