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InflamCellDeath SIGNED

Mechanism and function of gasdermin-induced inflammatory cell death

Total Cost €

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EC-Contrib. €

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Partnership

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 InflamCellDeath project word cloud

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

regulate    family    pro    forms    substrate    plasma    protein    cytokines    danger    terminal    larger    gasdermin    restricting    microbial    single    chronic    death    anti    pyroptotic    promotes    permeability    inflammasomes    function    noxious    immune    receptors    generates    cytotoxic    infection    defense    signalling    pores    platforms    necrotic    gasdermins    share    substances    signals    appear    cytosolic    pattern    pore    assembled    regulation    mechanism    group    release    inflammation    cleavage    diseases    therapies    regulators    antimicrobial    repair    programmed    found    activation    host    effectors    pathogen    activated    caused    membrane    caspase    fragment    comprehensively    leaderless    disease    innate    inflammatory    injury    pyroptosis    lytic    causes    detrimental    concomitant    cell    detection    characterizing    dependent    elucidate    members    recognition    bacterial    infectious    proteases    caspases    inflammasome    forming   

Project "InflamCellDeath" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITE DE LAUSANNE 

Organization address
address: Quartier Unil-Centre Bâtiment Unicentre
city: LAUSANNE
postcode: 1015
website: www.unil.ch

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 Switzerland [CH]
 Total cost 1˙999˙176 €
 EC max contribution 1˙999˙176 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2017-COG
 Funding Scheme ERC-COG
 Starting year 2018
 Duration (year-month-day) from 2018-03-01   to  2023-02-28

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITE DE LAUSANNE CH (LAUSANNE) coordinator 1˙999˙176.00

Map

 Project objective

Pyroptosis is a lytic pro-inflammatory type of programmed cell death that is induced by inflammatory caspases, a family of proteases that control the innate immune response to infection, injury or noxious substances. Inflammatory caspases are activated within so-called inflammasomes, cytosolic signalling platforms that are assembled by pattern recognition receptors upon the detection of pathogen- or host-derived danger signals. Pyroptosis is essential for antimicrobial host defense, but also promotes the concomitant release of inflammatory danger signals and leaderless cytokines that is detrimental during chronic inflammatory disease.

Recently it was found that pyroptosis is caused by the cleavage of a single caspase substrate called gasdermin-D. This cleavage generates a cytotoxic N-terminal fragment of gasdermin-D that targets the plasma membrane, where it forms large permeability pores and thus causes pyroptotic cell death. Gasdermin-D is only one member of the larger gasdermin protein family, an emerging group of cell death effectors that share its pore-forming cytotoxic activity and that appear to be major regulators of inflammatory necrotic cell death.

The main goal of this proposal is to comprehensively characterize the function of gasdermins in anti-microbial host defense, to investigate the consequences of gasdermin-D pore formation to the host cell and to elucidate the pathways that regulate gasdermin activation. My objectives are:

1) to define the role of gasdermin-D in inflammasome-dependent anti-bacterial host defense 2) to study the role of membrane repair in restricting gasdermin-D-induced membrane 3) to characterize the function and regulation of other gasdermin family members during infection

By characterizing the mechanism and function of gasdermin-induced cell death in host-defense and inflammation this project may contribute to the development of novel therapies for infectious as well as inflammatory diseases.

 Publications

year authors and title journal last update
List of publications.
2018 Sebastian Rühl, Kateryna Shkarina, Benjamin Demarco, Rosalie Heilig, José Carlos Santos, Petr Broz
ESCRT-dependent membrane repair negatively regulates pyroptosis downstream of GSDMD activation
published pages: 956-960, ISSN: 0036-8075, DOI: 10.1126/science.aar7607
Science 362/6417 2019-10-07
2019 Kaiwen W. Chen, Benjamin Demarco, Petr Broz
Pannexin‐1 promotes NLRP3 activation during apoptosis but is dispensable for canonical or noncanonical inflammasome activation
published pages: , ISSN: 0014-2980, DOI: 10.1002/eji.201948254
European Journal of Immunology 2019-10-07
2019 Kaiwen W. Chen, Dave Boucher, Petr Broz
Divide to conquer: NLRP3 is activated on dispersed trans-Golgi network
published pages: 181-182, ISSN: 1001-0602, DOI: 10.1038/s41422-018-0138-z
Cell Research 29/3 2019-10-07
2019 Kaiwen W Chen, Benjamin Demarco, Rosalie Heilig, Kateryna Shkarina, Andreas Boettcher, Christopher J Farady, Pawel Pelczar, Petr Broz
Extrinsic and intrinsic apoptosis activate pannexin‐1 to drive NLRP 3 inflammasome assembly
published pages: , ISSN: 0261-4189, DOI: 10.15252/embj.2019101638
The EMBO Journal 38/10 2019-10-07
2019 Benjamin Demarco, Kaiwen W. Chen, Petr Broz
Pannexin-1 channels bridge apoptosis to NLRP3 inflammasome activation
published pages: 1610324, ISSN: 2372-3556, DOI: 10.1080/23723556.2019.1610324
Molecular & Cellular Oncology 6/4 2019-10-07

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

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