FLAMMASEC

"Inflammasome-induced IL-1 Secretion: Route, Mechanism, and Cell Fate"

 Coordinatore KLINIKUM RECHTS DER ISAR DER TECHNISCHEN UNIVERSITAT MUNCHEN 

Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.

 Nazionalità Coordinatore Germany [DE]
 Totale costo 1˙495˙533 €
 EC contributo 1˙495˙533 €
 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) 2014-03-01   -   2019-02-28

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    KLINIKUM RECHTS DER ISAR DER TECHNISCHEN UNIVERSITAT MUNCHEN

 Organization address address: ISMANINGER STRASSE 22
city: MUENCHEN
postcode: 81675

contact info
Titolo: Dr.
Nome: Olaf
Cognome: Groß
Email: send email
Telefono: +49 89 4140 4874
Fax: +49 89 4140 4080

DE (MUENCHEN) hostInstitution 1˙495˙533.00
2    KLINIKUM RECHTS DER ISAR DER TECHNISCHEN UNIVERSITAT MUNCHEN

 Organization address address: ISMANINGER STRASSE 22
city: MUENCHEN
postcode: 81675

contact info
Titolo: Ms.
Nome: Beate
Cognome: Schaulin
Email: send email
Telefono: +49894140 2856
Fax: +49894140 4926

DE (MUENCHEN) hostInstitution 1˙495˙533.00

Mappa


 Word cloud

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

host    caspase    dependent    protease    beta    mechanism    route    inflammation    inflammasomes    inflammasome    secretion    mediated    hereditary    il    diseases   

 Obiettivo del progetto (Objective)

'Inflammasomes are intracellular danger-sensing protein complexes that are important for host protection. They initiate inflammation by controlling the activity of the proinflammatory cytokine interleukin-1β (IL-1β). Unlike most other cytokines, IL-1β is produced and retained in the cytoplasm in an inactive pro-form. Inflammasome-dependent maturation of proIL-1β is mediated by the common component of all inflammasomes, the protease caspase-1. Caspase-1 also controls the secretion of IL-1β, but the mechanism and route of secretion are unknown. We have recently demonstrated that the ability of caspase-1 to control IL-1β secretion is not dependent on its protease activity, but rather on a scaffold or adapter function of caspase-1. Furthermore, we and others could show that caspase-1 can control the secretion of non-substrates like IL-1α. These insights provide us with new and potentially revealing means to investigate the downstream effector functions of caspase-1, including the route and mechanism of IL-1 secretion. We will develop new tools to study the process of IL-1 secretion by microscopy and the novel mode-of-action of caspase-1 through the generation of transgenic models. Despite the important role of IL-1 in host defence against infection, dysregulated inflammasome activation and IL-1 production has a causal role in a number of acquired and hereditary auto-inflammatory conditions. These include particle-induced sterile inflammation (as is seen in gout and asbestosis), hereditary periodic fever syndromes, and metabolic diseases like diabetes and atherosclerosis. Currently, recombinant proteins that block the IL-1 receptor or deplete secreted IL-1 are used to treat IL-1-dependent diseases. These are costly treatments, and are also therapeutically cumbersome since they are not orally available. We hope that a better understanding of caspase-1-mediated secretion of IL-1 will unveil mechanisms that may serve as targets for future therapies for these diseases.'

Altri progetti dello stesso programma (FP7-IDEAS-ERC)

SHYNE (2012)

Stellar HYdrodynamics Nucleosynthesis and Evolution

Read More  

STEMCELLADAPT (2011)

Decoding the environmental adaptation of plant stem cell control

Read More  

BIOMIM (2011)

Biomimetic films and membranes as advanced materials for studies on cellular processes

Read More