ASC filament formation serves as a signal amplification mechanism for inflammasomes
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Pyk2 activates the NLRP3 inflammasome by directly phosphorylating ASC and contributes to inflammasome-dependent peritonitisGSDMD membrane pore formation constitutes the mechanism of pyroptotic cell deathEnzymatically Inactive Procaspase 1 stabilizes the ASC Pyroptosome and Supports Pyroptosome Spreading during Cell DivisionAssembly and regulation of ASC specks.Mechanisms governing inflammasome activation, assembly and pyroptosis induction.Lytic cell death induced by melittin bypasses pyroptosis but induces NLRP3 inflammasome activation and IL-1β release.The AIM2 inflammasome: Sensor of pathogens and cellular perturbations.Detection of ASC Oligomerization by Western Blotting.Negative regulation of MAVS-mediated innate immune response by ASC.In vivo evidence of inflammasome activation during spontaneous labor at term.Increased autophagic sequestration in adaptor protein-3 deficient dendritic cells limits inflammasome activity and impairs antibacterial immunity.The intra- and extracellular functions of ASC specks.COPs and POPs Patrol Inflammasome Activation.Identification of a selective and direct NLRP3 inhibitor to treat inflammatory disorders.Microglia-derived ASC specks cross-seed amyloid-β in Alzheimer's disease.MLKL forms disulfide bond-dependent amyloid-like polymers to induce necroptosis.Activation of the Innate Immune Receptors: Guardians of the Micro Galaxy : Activation and Functions of the Innate Immune Receptors.Zebrafish earns its stripes for in vivo ASC speck dynamics.Dynamics of in vivo ASC speck formation.Function and mechanism of the pyrin inflammasome.Emerging Concepts in Innate Immunity.LPS targets host guanylate-binding proteins to the bacterial outer membrane for non-canonical inflammasome activation.Caspase-1 self-cleavage is an intrinsic mechanism to terminate inflammasome activity.Artemisia Extract Suppresses NLRP3 and AIM2 Inflammasome Activation by Inhibition of ASC Phosphorylation.Tranilast directly targets NLRP3 to treat inflammasome-driven diseases.Development of a characterised tool kit for the interrogation of NLRP3 inflammasome-dependent responses.Oridonin is a covalent NLRP3 inhibitor with strong anti-inflammasome activity.Spotlight on the NLRP3 inflammasome pathwayThe inflammasomes, immune guardians at defence barriersA Founder Mutation Disrupts NF-κB Signaling by Inhibiting BCL10 and MALT1 Recruitment and Signalosome Formation
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ASC filament formation serves as a signal amplification mechanism for inflammasomes
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article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on 22 June 2016
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
ASC filament formation serves as a signal amplification mechanism for inflammasomes
@en
ASC filament formation serves as a signal amplification mechanism for inflammasomes.
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ASC filament formation serves as a signal amplification mechanism for inflammasomes
@en
ASC filament formation serves as a signal amplification mechanism for inflammasomes.
@nl
prefLabel
ASC filament formation serves as a signal amplification mechanism for inflammasomes
@en
ASC filament formation serves as a signal amplification mechanism for inflammasomes.
@nl
P2860
P50
P356
P1476
ASC filament formation serves as a signal amplification mechanism for inflammasomes
@en
P2093
Lorenzo Sborgi
Sebastian Rühl
P2507
P2860
P2888
P356
10.1038/NCOMMS11929
P407
P577
2016-06-22T00:00:00Z