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BATTLE

The molecular basis of NleB-mediated bacterial virulence

Total Cost €

EC-Contrib. €

Partnership

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Outcomes and
results

BATTLE project word cloud

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

shown protein ways cell virulence inhibitors colonization generate signalling glycosyltransferase glcnacylation apoptosis binding enterohemorrhagic thereby enteropathogenic enteric mechanisms recognises salmonella proteins infection intestinal effector escherichia secretion nleb prevents utilize colonizing molecular containing interfere shigella antimicrobial domains coli uncover interact glcnacylate human cells arginine inhibiting bacterial bisubstrate effectors pathogens receptor death domain preventing host

Project "BATTLE" data sheet

The following table provides information about the project.

Coordinator	UNIVERSITY OF DUNDEE Organization address address: Nethergate city: DUNDEE postcode: DD1 4HN website: www.dundee.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]
Project website	https://www.sites.google.com/site/vanaaltenlab/the-team
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-2014
Funding Scheme	MSCA-IF-EF-ST
Starting year	2016
Duration (year-month-day)	from 2016-01-04 to 2018-01-03

Partnership

Take a look of project's partnership.

#	participants	country	role	EC contrib. [€]
1	UNIVERSITY OF DUNDEE UNIVERSITY OF DUNDEE Organization address address: Nethergate city: DUNDEE postcode: DD1 4HN website: www.dundee.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.	UK (DUNDEE)	coordinator	183˙454.00

Map

Project objective

Bacterial pathogens have evolved distinct ways of colonizing host cells and promote infection. Many human intestinal bacterial pathogens such as Salmonella, Shigella and enteropathogenic/ enterohemorrhagic Escherichia coli utilize type III secretion systems to deliver virulence effector proteins into the host to promote colonization and interfere with antimicrobial host response. Among the type III effectors, the NleB protein has been shown to be essential for virulence of enteric pathogens. NleB is a glycosyltransferase that has been shown to interact with host cell death-domain-containing proteins, GlcNAcylate a specific arginine on these and thereby inhibiting death receptor signalling and preventing host cell apoptosis. This proposal will 1) investigate how NleB specifically recognises the host death domains, 2) uncover the molecular mechanisms of arginine GlcNAcylation, 3) explain how death domain GlcNAcylation prevents the death domain from binding to its receptor, and 4) exploit this molecular information to generate bisubstrate inhibitors to interfere with this process.

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