Mitochondrial apoptosis is dispensable for NLRP3 inflammasome activation but non-apoptotic caspase-8 is required for inflammasome priming - Wikidata - awgldk - TriplyDB

Mitochondrial apoptosis is dispensable for NLRP3 inflammasome activation but non-apoptotic caspase-8 is required for inflammasome priming

Mitochondrial apoptosis is dispensable for NLRP3 inflammasome activation but non-apoptotic caspase-8 is required for inflammasome priming

http://www.wikidata.org/entity/Q34343275

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The Reactive Oxygen Species in Macrophage Polarization: Reflecting Its Dual Role in Progression and Treatment of Human Diseases Converging roles of caspases in inflammasome activation, cell death and innate immunity DED or alive: assembly and regulation of the death effector domain complexes NADPH oxidase- and mitochondria-derived reactive oxygen species in proinflammatory microglial activation: a bipartisan affair?Inflammasomes: mechanism of action, role in disease, and therapeutics Mechanisms of inflammasome activation: recent advances and novel insights Old, new and emerging functions of caspases.Initiation and perpetuation of NLRP3 inflammasome activation and assembly The intersection of cell death and inflammasome activation Mitochondria: diversity in the regulation of the NLRP3 inflammasome.Pyrin inflammasome activation and RhoA signaling in the autoinflammatory diseases FMF and HIDS RIPK3 promotes cell death and NLRP3 inflammasome activation in the absence of MLKL The Pseudokinase MLKL and the Kinase RIPK3 Have Distinct Roles in Autoimmune Disease Caused by Loss of Death-Receptor-Induced Apoptosis.Keeping the immune system in check: a role for mitophagy.Cytosolic double-stranded RNA activates the NLRP3 inflammasome via MAVS-induced membrane permeabilization and K+ efflux.Inflammasome activation leads to Caspase-1-dependent mitochondrial damage and block of mitophagy.The necroptosis adaptor RIPK3 promotes injury-induced cytokine expression and tissue repair.Inflammasomes as polyvalent cell death platforms.TNFR1-dependent cell death drives inflammation in Sharpin-deficient mice.UCP2-induced fatty acid synthase promotes NLRP3 inflammasome activation during sepsis Modulation of SIV and HIV DNA vaccine immunity by Fas-FasL signaling K+ efflux agonists induce NLRP3 inflammasome activation independently of Ca2+ signaling.Regulation of inflammasome activation.Inhibitor of apoptosis proteins as intracellular signaling intermediates.Caspase-8 as an Effector and Regulator of NLRP3 Inflammasome Signaling Enhanced activity of NLRP3 inflammasome in peripheral blood cells of patients with active rheumatoid arthritis.Endoplasmic Reticulum Stress Activates the Inflammasome via NLRP3- and Caspase-2-Driven Mitochondrial Damage.Activity of Uncleaved Caspase-8 Controls Anti-bacterial Immune Defense and TLR-Induced Cytokine Production Independent of Cell Death Defective mitochondrial fission augments NLRP3 inflammasome activation New insights into the regulation of innate immunity by caspase-8.Caspase-11 Requires the Pannexin-1 Channel and the Purinergic P2X7 Pore to Mediate Pyroptosis and Endotoxic Shock.Caspase-8: not so silently deadly.Novel roles for caspase-8 in IL-1β and inflammasome regulation.NLRP3 at the interface of metabolism and inflammation.Mitochondria and the hallmarks of cancer.Necroptosis-independent signaling by the RIP kinases in inflammation.NLRP3 inflammasome activation downstream of cytoplasmic LPS recognition by both caspase-4 and caspase-5.Mitochondria and the NLRP3 inflammasome: physiological and pathological relevance.Mechanism and Regulation of NLRP3 Inflammasome Activation.A motive for killing: effector functions of regulated lytic cell death.

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P2860

Mitochondrial apoptosis is dispensable for NLRP3 inflammasome activation but non-apoptotic caspase-8 is required for inflammasome priming

http://www.wikidata.org/entity/Q34343275

description

2014 nî lūn-bûn

@nan

2014 թուականի Յուլիսին հրատարակուած գիտական յօդուած

@hyw

2014 թվականի հուլիսին հրատարակված գիտական հոդված

@hy

2014年の論文

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2014年論文

@yue

2014年論文

@zh-hant

2014年論文

@zh-hk

2014年論文

@zh-mo

2014年論文

@zh-tw

2014年论文

@wuu

name

Mitochondrial apoptosis is dis ...... uired for inflammasome priming

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Mitochondrial apoptosis is dis ...... uired for inflammasome priming

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Mitochondrial apoptosis is dis ...... uired for inflammasome priming

@nl

type

label

Mitochondrial apoptosis is dis ...... uired for inflammasome priming

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Mitochondrial apoptosis is dis ...... uired for inflammasome priming

@en

Mitochondrial apoptosis is dis ...... uired for inflammasome priming

@nl

prefLabel

Mitochondrial apoptosis is dis ...... uired for inflammasome priming

@ast

Mitochondrial apoptosis is dis ...... uired for inflammasome priming

@en

Mitochondrial apoptosis is dis ...... uired for inflammasome priming

@nl

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Mitochondrial apoptosis is dis ...... uired for inflammasome priming

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Alison L Mildenhall

http://www.w3.org/2001/XMLSchema#string

Donia M Moujalled

http://www.w3.org/2001/XMLSchema#string

Francine Ke

http://www.w3.org/2001/XMLSchema#string

James E Vince

http://www.w3.org/2001/XMLSchema#string

Lorraine A O'Reilly

http://www.w3.org/2001/XMLSchema#string

Rowena S Lewis

http://www.w3.org/2001/XMLSchema#string

Warren Alexander

http://www.w3.org/2001/XMLSchema#string

P2860

Activation of autophagy by inflammatory signals limits IL-1β production by targeting ubiquitinated inflammasomes for destruction

Parkin is recruited selectively to impaired mitochondria and promotes their autophagy

The adaptor MAVS promotes NLRP3 mitochondrial localization and inflammasome activation

The pseudokinase MLKL mediates necroptosis via a molecular switch mechanism

A role for mitochondria in NLRP3 inflammasome activation

Cyclophilin D-dependent mitochondrial permeability transition regulates some necrotic but not apoptotic cell death

Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death

Calcium signaling and mitochondrial destabilization in the triggering of the NLRP3 inflammasome

Intracellular localization of the BCL-2 family member BOK and functional implications

N-terminal fragment of c-FLIP(L) processed by caspase 8 specifically interacts with TRAF2 and induces activation of the NF-kappaB signaling pathway

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982-990

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scholarly article

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10.15252/EMBR.201438463

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9

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15

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Andreas Strasser

Katryn J. Stacey

Ramanjaneyulu Allam

Michael J. White

Benjamin T. Kile

Eric Chi-Wang Yu

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2014-07-02T00:00:00Z

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263710070

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24990442

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apoptotic process

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4198042

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