Explore the words cloud of the InflamCellDeath project. It provides you a very rough idea of what is the project "InflamCellDeath" about.
The following table provides information about the project.
UNIVERSITE DE LAUSANNE
|Coordinator Country||Switzerland [CH]|
|Total cost||1˙999˙176 €|
|EC max contribution||1˙999˙176 € (100%)|
1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
|Duration (year-month-day)||from 2018-03-01 to 2023-02-28|
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|1||UNIVERSITE DE LAUSANNE||CH (LAUSANNE)||coordinator||1˙999˙176.00|
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.
|year||authors and title||journal||last update|
Sebastian RÃ¼hl, Kateryna Shkarina, Benjamin Demarco, Rosalie Heilig, JosÃ© 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
Kaiwen W. Chen, Benjamin Demarco, Petr Broz
Pannexinâ€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|
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|
Kaiwen W Chen, Benjamin Demarco, Rosalie Heilig, Kateryna Shkarina, Andreas Boettcher, Christopher J Farady, Pawel Pelczar, Petr Broz
Extrinsic and intrinsic apoptosis activate pannexinâ€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|
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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