Deletion of FADD in macrophages and granulocytes results in RIP3- and MyD88-dependent systemic inflammation - Wikidata - awgldk - TriplyDB

Deletion of FADD in macrophages and granulocytes results in RIP3- and MyD88-dependent systemic inflammation

Deletion of FADD in macrophages and granulocytes results in RIP3- and MyD88-dependent systemic inflammation

http://www.wikidata.org/entity/Q35393485

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Conditional deletion of caspase-8 in macrophages alters macrophage activation in a RIPK-dependent manner.Fas Regulates Macrophage Polarization and Fibrogenic Phenotype in a Model of Chronic Ethanol-Induced Hepatocellular Injury.The inflammatory role of phagocyte apoptotic pathways in rheumatic diseases.The contribution of the programmed cell death machinery in innate immune cells to lupus nephritis.Caspase-8: regulating life and death.Expression Profile and Tissue-Specific Distribution of the Receptor-Interacting Protein 3 in BALB/c Mice.Necroptosis: Mechanisms and Relevance to Disease.

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P2860

Deletion of FADD in macrophages and granulocytes results in RIP3- and MyD88-dependent systemic inflammation

http://www.wikidata.org/entity/Q35393485

description

2015 nî lūn-bûn

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2015 թուականի Ապրիլին հրատարակուած գիտական յօդուած

@hyw

2015 թվականի ապրիլին հրատարակված գիտական հոդված

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2015年の論文

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2015年学术文章

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2015年学术文章

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2015年学术文章

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2015年学术文章

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2015年学术文章

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2015年學術文章

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name

Deletion of FADD in macrophage ...... ependent systemic inflammation

@ast

Deletion of FADD in macrophage ...... ependent systemic inflammation

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type

label

Deletion of FADD in macrophage ...... ependent systemic inflammation

@ast

Deletion of FADD in macrophage ...... ependent systemic inflammation

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prefLabel

Deletion of FADD in macrophage ...... ependent systemic inflammation

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Deletion of FADD in macrophage ...... ependent systemic inflammation

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Deletion of FADD in macrophage ...... ependent systemic inflammation

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Astar Winoto

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Jennifer A Young

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Suruchi N Schock

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Tina H He

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Yuefang Sun

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P2860

Fas triggers an alternative, caspase-8-independent cell death pathway using the kinase RIP as effector molecule

Receptor interacting protein kinase-3 determines cellular necrotic response to TNF-alpha

Phosphorylation-driven assembly of the RIP1-RIP3 complex regulates programmed necrosis and virus-induced inflammation

Apoptosis, pyroptosis, and necrosis: mechanistic description of dead and dying eukaryotic cells.

FADD and caspase-8 control the outcome of autophagic signaling in proliferating T cells

Programmed necrosis in the cross talk of cell death and inflammation

Type I interferon induces necroptosis in macrophages during infection with Salmonella enterica serovar Typhimurium

Catalytic activity of the caspase-8-FLIP(L) complex inhibits RIPK3-dependent necrosis

RIP3, an energy metabolism regulator that switches TNF-induced cell death from apoptosis to necrosis

In vivo depletion of CD11c+ dendritic cells abrogates priming of CD8+ T cells by exogenous cell-associated antigens

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