SUMOFLU

Interplay between influenza viruses and host SUMO pathways

 Coordinatore UNIVERSITAET ZUERICH 

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 Nazionalità Coordinatore Switzerland [CH]
 Totale costo 1˙482˙452 €
 EC contributo 1˙482˙452 €
 Programma FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call ERC-2013-StG
 Funding Scheme ERC-SG
 Anno di inizio 2014
 Periodo (anno-mese-giorno) 2014-02-01   -   2019-01-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITY OF GLASGOW

 Organization address address: University Avenue
city: GLASGOW
postcode: G12 8QQ

contact info
Titolo: Mr.
Nome: Joseph
Cognome: Galloway
Email: send email
Telefono: +44 141 330 3884
Fax: +44 141 330 5611

UK (GLASGOW) beneficiary 0.00
2    UNIVERSITAET ZUERICH

 Organization address address: Raemistrasse 71
city: ZURICH
postcode: 8006

contact info
Titolo: Dr.
Nome: Benjamin
Cognome: Hale
Email: send email
Telefono: +41 44 634 2899
Fax: +41 44 634 4967

CH (ZURICH) hostInstitution 1˙482˙452.00
3    UNIVERSITAET ZUERICH

 Organization address address: Raemistrasse 71
city: ZURICH
postcode: 8006

contact info
Titolo: Ms.
Nome: Monika
Cognome: Wiget
Email: send email
Telefono: +41 44 634 5350

CH (ZURICH) hostInstitution 1˙482˙452.00

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

virus    mechanisms    antivirals    function    infection    pathways    cell    sumoylation    host    enzymes    proteins    influenza    components    identification    conjugation    fundamental    resistance    replication    biology    cellular    viruses    sumo   

 Obiettivo del progetto (Objective)

'Influenza viruses cause a significant seasonal disease burden and continually threaten to initiate human pandemics. Antivirals are available for treatment of influenza, however drug-resistant viruses often emerge. Thus, there is urgent need to develop new antivirals with lower chances of selecting resistance. As viruses rely extensively on cellular functions, one way to minimise resistance is to target new antivirals against host factors. This concept requires a fundamental understanding of mechanisms underpinning the interplay between influenza viruses and their hosts.

In this project, we will investigate the role that host SUMO pathways play during influenza virus replication. SUMO proteins are important regulators of cell signalling, and are covalently linked to other proteins in order to alter structure, localization or function. As such, SUMO conjugation regulates many diverse aspects of biology. Our own work shows that global cellular SUMOylation increases during influenza virus infection, and that virus replication is severely impaired when cells are depleted of key enzymes and components required for general SUMO conjugation. Here, we will determine what viral components trigger SUMOylation, and which specific cellular enzymes are involved. We will characterize where in the cell SUMO conjugates accumulate, and for the first time apply large-scale affinity-based quantitative proteomics to the identification of proteins that become SUMO modified during infection. A key aim will be to correlate changes to the SUMO sub-proteome with the function of specific host SUMO-modifying enzymes, thereby establishing the mechanistic role of these modifications during virus replication.

Understanding basic mechanisms underlying SUMOylation during influenza virus infection will provide new insights into the fundamental biology of these important pathogens. The work could also lead to identification of key cellular pathways that can be exploited as novel therapeutic targets'

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