Apoptosis induced by the toll-like receptor adaptor TRIF is dependent on its receptor interacting protein homotypic interaction motif
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The RIP1/RIP3 necrosome forms a functional amyloid signaling complex required for programmed necrosiscIAPs block Ripoptosome formation, a RIP1/caspase-8 containing intracellular cell death complex differentially regulated by cFLIP isoformsAn outline of necrosome triggersConcepts and mechanisms underlying chemotherapy induced immunogenic cell death: impact on clinical studies and considerations for combined therapiesDeath in the fast lane: what's next for necroptosis?The two faces of receptor interacting protein kinase-1The effects of TLR activation on T-cell development and differentiationProgrammed necrosis in the cross talk of cell death and inflammationThe TLR signalling adaptor TRIF/TICAM-1 has an N-terminal helical domain with structural similarity to IFIT proteinsPeli1 facilitates TRIF-dependent Toll-like receptor signaling and proinflammatory cytokine productionMyD88-5 links mitochondria, microtubules, and JNK3 in neurons and regulates neuronal survivalCaspase inhibitors protect neurons by enabling selective necroptosis of inflamed microgliaReceptor-interacting protein homotypic interaction motif-dependent control of NF-kappa B activation via the DNA-dependent activator of IFN regulatory factorsPoly I:C enhances cycloheximide-induced apoptosis of tumor cells through TLR3 pathwayRetaining MKP1 expression and attenuating JNK-mediated apoptosis by RIP1 for cisplatin resistance through miR-940 inhibitionThree-tier regulation of cell number plasticity by neurotrophins and Tolls in Drosophila.Caspase-8 mediates caspase-1 processing and innate immune defense in response to bacterial blockade of NF-κB and MAPK signalingRIP1 suppresses innate immune necrotic as well as apoptotic cell death during mammalian parturition.A new domain in the Toll/IL-1R domain-containing adaptor inducing interferon-β factor protein amino terminus is important for tumor necrosis factor-α receptor-associated factor 3 association, protein stabilization and interferon signaling.Analysis of a TIR-less splice variant of TRIF reveals an unexpected mechanism of TLR3-mediated signalingThe coxsackievirus B 3C protease cleaves MAVS and TRIF to attenuate host type I interferon and apoptotic signalingTRIF modulates TLR5-dependent responses by inducing proteolytic degradation of TLR5The molecular regulation of programmed necrotic cell injury.Immunomodulatory effects of dsRNA and its potential as vaccine adjuvant.Disruption of TLR3 signaling due to cleavage of TRIF by the hepatitis A virus protease-polymerase processing intermediate, 3CD.Lipopolysaccharide potentiates effector T cell accumulation into nonlymphoid tissues through TRIFCharacterization of dsRNA-induced pancreatitis model reveals the regulatory role of IFN regulatory factor 2 (Irf2) in trypsinogen5 gene transcription.Regulation of MyD88 aggregation and the MyD88-dependent signaling pathway by sequestosome 1 and histone deacetylase 6Necroptotic signaling in adaptive and innate immunity.TRIF licenses caspase-11-dependent NLRP3 inflammasome activation by gram-negative bacteria.RIP kinases: key decision makers in cell death and innate immunity.Activation of TLR3 promotes the degeneration of retinal ganglion cells by upregulating the protein levels of JNK3Toll-like receptor, RIG-I-like receptors and the NLRP3 inflammasome: key modulators of innate immune responses to double-stranded RNA viruses.Cellular mechanisms of toll-like receptor-3 activation in the thalamus are associated with white matter injury in the developing brainThe ribonucleotide reductase R1 subunits of herpes simplex virus 1 and 2 protect cells against poly(I · C)-induced apoptosisCharacterization of bbtTICAM from amphioxus suggests the emergence of a MyD88-independent pathway in basal chordatesSuppression of RIP3-dependent necroptosis by human cytomegalovirusHerpes simplex encephalitis in children with autosomal recessive and dominant TRIF deficiencyEngagement of Fas on Macrophages Modulates Poly I:C induced cytokine production with specific enhancement of IP-10.TLR3 expression correlates with apoptosis, proliferation and angiogenesis in hepatocellular carcinoma and predicts prognosis
P2860
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P2860
Apoptosis induced by the toll-like receptor adaptor TRIF is dependent on its receptor interacting protein homotypic interaction motif
description
2005 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
2005 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
artículu científicu espublizáu en 2005
@ast
im April 2005 veröffentlichter wissenschaftlicher Artikel
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scientific journal article
@en
vedecký článok (publikovaný 2005/04/15)
@sk
vědecký článek publikovaný v roce 2005
@cs
wetenschappelijk artikel (gepubliceerd op 2005/04/15)
@nl
наукова стаття, опублікована у квітні 2005
@uk
مقالة علمية (نشرت في 15-4-2005)
@ar
name
Apoptosis induced by the toll- ...... in homotypic interaction motif
@ast
Apoptosis induced by the toll- ...... in homotypic interaction motif
@en
Apoptosis induced by the toll- ...... in homotypic interaction motif
@nl
type
label
Apoptosis induced by the toll- ...... in homotypic interaction motif
@ast
Apoptosis induced by the toll- ...... in homotypic interaction motif
@en
Apoptosis induced by the toll- ...... in homotypic interaction motif
@nl
prefLabel
Apoptosis induced by the toll- ...... in homotypic interaction motif
@ast
Apoptosis induced by the toll- ...... in homotypic interaction motif
@en
Apoptosis induced by the toll- ...... in homotypic interaction motif
@nl
P3181
P1476
Apoptosis induced by the toll- ...... in homotypic interaction motif
@en
P2093
Margaret K. Offermann
William J. Kaiser
P304
P3181
P356
10.4049/JIMMUNOL.174.8.4942
P407
P577
2005-04-15T00:00:00Z