Structure-Function Analysis of the Chemokine Interactome for Therapeutic Targeting and Imaging in Atherosclerosis


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 Nazionalità Coordinatore Germany [DE]
 Totale costo 2˙500˙000 €
 EC contributo 2˙500˙000 €
 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-2009-AdG
 Funding Scheme ERC-AG
 Anno di inizio 2010
 Periodo (anno-mese-giorno) 2010-04-01   -   2016-03-31


# participant  country  role  EC contrib. [€] 

 Organization address address: Pauwelsstrasse 30
city: AACHEN
postcode: 52074

contact info
Titolo: Mr.
Nome: Volker
Cognome: Legewie
Email: send email
Telefono: +49 241 80 88494
Fax: +49 241 80 82051

DE (AACHEN) beneficiary 0.00

 Organization address address: GESCHWISTER SCHOLL PLATZ 1
postcode: 80539

contact info
Titolo: Mr.
Nome: Danny
Cognome: Duhme
Email: send email
Telefono: +49 89 2180 3449
Fax: +49 89 2180 2985

DE (MUENCHEN) hostInstitution 2˙500˙000.00

 Organization address address: GESCHWISTER SCHOLL PLATZ 1
postcode: 80539

contact info
Titolo: Prof.
Nome: Christian
Cognome: Weber
Email: send email
Telefono: +49 89 5160 4350
Fax: +49 89 5160 4352

DE (MUENCHEN) hostInstitution 2˙500˙000.00


 Word cloud

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atherosclerosis    linked    disease    chemokine    heteromers    vivo    functional    heteromerization    generate    binding    chemokines    heterodimers    inflammatory    peptides   

 Obiettivo del progetto (Objective)

'Atherosclerosis is characterized by chronic inflammation of the arterial wall. Mononuclear cell recruitment is driven by chemokines that can be deposited e.g. by activated platelets on inflamed endothelium. Chemokines require oligomerization and immobilization for efficient function, and recent evidence supports the notion that heterodimer formation between chemokines constitutes a new regulatory principle amplifying specific chemokine activities while suppressing others. Although crucial to inflammatory disease, this has been difficult to prove in vivo, primarily as chemokine heterodimers exist in equilibrium with their homodimer counterparts. We introduce the paradigm that heteromerization of chemokines provides the combinatorial diversity for functional plasticity and fine-tuning, coining this interactome. Given the relevance of chemokine heteromers in vivo, we aim to exploit this in an anti-inflammatory approach to selectively target vascular disease. In a multidisciplinary project, we plan to generate covalently-linked heterodimers to establish their biological significance. Obligate heterodimers of CC and CXC chemokines will be designed using computer-assisted modeling, chemically synthesized and cross-linked, structurally assessed using NMR spectroscopy and crystallography, and subjected to functional characterization in vitro and reconstitution in vivo. Conversely, we will develop cyclic beta-sheet-based peptides binding chemokines to specifically disrupt heteromers and we will generate mice with conditional deletion or knock-in of chemokine mutants with defects in heteromerization or proteoglycan binding to be analyzed in models of atherosclerosis. Peptides will be used for molecular imaging and chemokine heteromers will be quantified in cardiovascular patients.'

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