Mechanism of impaired NLRP3 inflammasome priming by monophosphoryl lipid A. - Wikidata - wikimedia - TriplyDB

Mechanism of impaired NLRP3 inflammasome priming by monophosphoryl lipid A.

Mechanism of impaired NLRP3 inflammasome priming by monophosphoryl lipid A.

http://www.wikidata.org/entity/Q40093877

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Immune response to vaccine adjuvants during the first year of life CD36 coordinates NLRP3 inflammasome activation by facilitating intracellular nucleation of soluble ligands into particulate ligands in sterile inflammation The ultra-potent and selective TLR8 agonist VTX-294 activates human newborn and adult leukocytes.Inefficient TLR4/MD-2 heterotetramerization by monophosphoryl lipid A Nedd8 regulates inflammasome-dependent caspase-1 activation.IKKα negatively regulates ASC-dependent inflammasome activation.Type I interferon signaling contributes to the bias that Toll-like receptor 4 exhibits for signaling mediated by the adaptor protein TRIF.Caspase-1 Dependent IL-1β Secretion and Antigen-Specific T-Cell Activation by the Novel Adjuvant, PCEP.Effects of Differences in Lipid A Structure on TLR4 Pro-Inflammatory Signaling and Inflammasome Activation.Sensing and reacting to microbes through the inflammasomes.Toll-like receptor 4-interacting SPA4 peptide suppresses the NLRP3 inflammasome in response to LPS and ATP stimuli Selective TRIF-dependent signaling by a synthetic toll-like receptor 4 agonist.Adjuvant activity of naturally occurring monophosphoryl lipopolysaccharide preparations from mucosa-associated bacteria Comparative Transcriptome Profiles of Human Blood in Response to the Toll-like Receptor 4 Ligands Lipopolysaccharide and Monophosphoryl Lipid A.Immunology in clinic review series; focus on autoinflammatory diseases: role of inflammasomes in autoinflammatory syndromes.Pattern recognition receptors: sentinels in innate immunity and targets of new vaccine adjuvants.Mechanisms of action of adjuvants TRIM32-TAX1BP1-dependent selective autophagic degradation of TRIF negatively regulates TLR3/4-mediated innate immune responses.Mitochondria-targeted drugs enhance Nlrp3 inflammasome-dependent IL-1β secretion in association with alterations in cellular redox and energy status.Naturally occurring low biological reactivity lipopolysaccharides as vaccine adjuvants.Specific features of human monocytes activation by monophosphoryl lipid A.

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P2860

Mechanism of impaired NLRP3 inflammasome priming by monophosphoryl lipid A.

http://www.wikidata.org/entity/Q40093877

description

2011 nî lūn-bûn

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

@zh-mo

2011年論文

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2011年论文

@wuu

2011年论文

@zh

2011年论文

@zh-cn

name

Mechanism of impaired NLRP3 inflammasome priming by monophosphoryl lipid A.

@en

type

label

Mechanism of impaired NLRP3 inflammasome priming by monophosphoryl lipid A.

@en

prefLabel

Mechanism of impaired NLRP3 inflammasome priming by monophosphoryl lipid A.

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Mechanism of impaired NLRP3 inflammasome priming by monophosphoryl lipid A.

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Chelsea A Embry

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Gabriel Nuñez

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Luigi Franchi

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Thomas C Mitchell

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P2860

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A novel heterodimeric cysteine protease is required for interleukin-1 beta processing in monocytes

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Activation of inflammasomes requires intracellular redistribution of the apoptotic speck-like protein containing a caspase recruitment domain

A NOD2-NALP1 complex mediates caspase-1-dependent IL-1beta secretion in response to Bacillus anthracis infection and muramyl dipeptide

P2X7 receptor differentially couples to distinct release pathways for IL-1beta in mouse macrophage

Loss of the autophagy protein Atg16L1 enhances endotoxin-induced IL-1beta production

Cutting edge: NF-kappaB activating pattern recognition and cytokine receptors license NLRP3 inflammasome activation by regulating NLRP3 expression

The inflammasome: a caspase-1-activation platform that regulates immune responses and disease pathogenesis

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