Toll-like receptor 3-mediated necrosis via TRIF, RIP3, and MLKL. - Wikidata - wikimedia - TriplyDB

Toll-like receptor 3-mediated necrosis via TRIF, RIP3, and MLKL.

Toll-like receptor 3-mediated necrosis via TRIF, RIP3, and MLKL.

http://www.wikidata.org/entity/Q37312225

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Insights into the evolution of divergent nucleotide-binding mechanisms among pseudokinases revealed by crystal structures of human and mouse MLKL Necroptosis in tumorigenesis, activation of anti-tumor immunity, and cancer therapy Molecular crosstalk between apoptosis, necroptosis, and survival signaling Poly-ubiquitination in TNFR1-mediated necroptosis An outline of necrosome triggers Necroptosis in acute kidney injury: a shedding light The two faces of receptor interacting protein kinase-1 Ubiquitin in the immune system Execution of RIPK3-regulated necrosis Programmed necrosis in the cross talk of cell death and inflammation Casp8p41: The Protean Mediator of Death in CD4 T-cells that Replicate HIV The role of necroptosis in neurosurgical diseases Emerging therapies targeting intra-organ inflammation in transplantation Necroptosis: The Trojan horse in cell autonomous antiviral host defense Herpes Simplex Virus 1 (HSV-1) and HSV-2 Mediate Species-Specific Modulations of Programmed Necrosis through the Viral Ribonucleotide Reductase Large Subunit R1 Ppm1b negatively regulates necroptosis through dephosphorylating Rip3 Distinct roles of RIP1-RIP3 hetero- and RIP3-RIP3 homo-interaction in mediating necroptosis A cellular screen identifies ponatinib and pazopanib as inhibitors of necroptosis.Essential versus accessory aspects of cell death: recommendations of the NCCD 2015.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.Toll-like receptor-mediated down-regulation of the deubiquitinase cylindromatosis (CYLD) protects macrophages from necroptosis in wild-derived mice Caspase-8 and RIP kinases regulate bacteria-induced innate immune responses and cell death.RIP1 suppresses innate immune necrotic as well as apoptotic cell death during mammalian parturition.The Absence of Interferon-β Promotor Stimulator-1 (IPS-1) Predisposes to Bronchiolitis and Asthma-like Pathology in Response to Pneumoviral Infection in Mice RIPK1 blocks early postnatal lethality mediated by caspase-8 and RIPK3 Autophagy and its link to type II diabetes mellitus Mechanisms of acetaminophen hepatotoxicity and their translation to the human pathophysiology.Regulation of necrotic cell death: p53, PARP1 and cyclophilin D-overlapping pathways of regulated necrosis?Cutting edge: RIPK1 Kinase inactive mice are viable and protected from TNF-induced necroptosis in vivo Type-I interferon signaling through ISGF3 complex is required for sustained Rip3 activation and necroptosis in macrophages.Programmed cell death and its role in inflammation Fight or flight: regulation of emergency hematopoiesis by pyroptosis and necroptosis.Hematopoietic RIPK1 deficiency results in bone marrow failure caused by apoptosis and RIPK3-mediated necroptosis.Direct activation of RIP3/MLKL-dependent necrosis by herpes simplex virus 1 (HSV-1) protein ICP6 triggers host antiviral defense.The necroptosis adaptor RIPK3 promotes injury-induced cytokine expression and tissue repair.Programmed necrosis in inflammation: Toward identification of the effector molecules.Regulated cell death in AKI.RIP kinases: key decision makers in cell death and innate immunity.A20 restricts ubiquitination of pro-interleukin-1β protein complexes and suppresses NLRP3 inflammasome activity.

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Toll-like receptor 3-mediated necrosis via TRIF, RIP3, and MLKL.

http://www.wikidata.org/entity/Q37312225

description

article científic

@ca

article scientifique

@fr

articolo scientifico

@it

artigo científico

@pt

bilimsel makale

@tr

scientific article published on 09 September 2013

@en

vedecký článok

@sk

vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

Toll-like receptor 3-mediated necrosis via TRIF, RIP3, and MLKL.

@en

Toll-like receptor 3-mediated necrosis via TRIF, RIP3, and MLKL.

@nl

type

label

Toll-like receptor 3-mediated necrosis via TRIF, RIP3, and MLKL.

@en

Toll-like receptor 3-mediated necrosis via TRIF, RIP3, and MLKL.

@nl

prefLabel

Toll-like receptor 3-mediated necrosis via TRIF, RIP3, and MLKL.

@en

Toll-like receptor 3-mediated necrosis via TRIF, RIP3, and MLKL.

@nl

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P356

JBC.M113.462341

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Journal of Biological Chemistry

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Toll-like receptor 3-mediated necrosis via TRIF, RIP3, and MLKL.

@en

P2093

Chunzi Huang

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

Clark A Sehon

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

Edward S Mocarski

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

Haripriya Sridharan

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

Jason W Upton

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

John Bertin

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

Peter J Gough

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

Pratyusha Mandal

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

Robert W Marquis

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

William J Kaiser

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

P2860

Cleavage of the death domain kinase RIP by caspase-8 prompts TNF-induced apoptosis

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

The RIP1/RIP3 necrosome forms a functional amyloid signaling complex required for programmed necrosis

Mixed lineage kinase domain-like protein mediates necrosis signaling downstream of RIP3 kinase

The mitochondrial phosphatase PGAM5 functions at the convergence point of multiple necrotic death pathways

cIAPs block Ripoptosome formation, a RIP1/caspase-8 containing intracellular cell death complex differentially regulated by cFLIP isoforms

DAI/ZBP1 recruits RIP1 and RIP3 through RIP homotypic interaction motifs to activate NF-kappaB

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

Toll-like receptors 9 and 3 as essential components of innate immune defense against mouse cytomegalovirus infection

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31268-31279

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scholarly article

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10.1074/JBC.M113.462341

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P433

43

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288

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2013-09-09T00:00:00Z

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24019532

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Toll-like receptor

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3829437

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