MD-2 is required for disulfide HMGB1-dependent TLR4 signaling. - Wikidata - wikimedia - TriplyDB

MD-2 is required for disulfide HMGB1-dependent TLR4 signaling.

MD-2 is required for disulfide HMGB1-dependent TLR4 signaling.

http://www.wikidata.org/entity/Q34924679

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Multiple Targets of Salicylic Acid and Its Derivatives in Plants and Animals The Toll of Vascular Insufficiency: Implications for the Management of Peripheral Arterial Disease DAMPs from Cell Death to New Life Stress sounds the alarmin: The role of the danger-associated molecular pattern HMGB1 in stress-induced neuroinflammatory priming DAMPs, MAMPs, and NAMPs in plant innate immunity Trial Watch: Immunostimulation with Toll-like receptor agonists in cancer therapy Aspirin's Active Metabolite Salicylic Acid Targets High Mobility Group Box 1 to Modulate Inflammatory Responses Anemia of Inflammation: A Review.Ethanol, TLR3, and TLR4 Agonists Have Unique Innate Immune Responses in Neuron-Like SH-SY5Y and Microglia-Like BV2 An ongoing search for potential targets and therapies for lethal sepsis Activation of Plant Innate Immunity by Extracellular High Mobility Group Box 3 and Its Inhibition by Salicylic Acid.Toll-like receptor 4 signaling: A common pathway for interactions between prooxidants and extracellular disulfide high mobility group box 1 (HMGB1) protein-coupled activation.Serum Amyloid A Stimulates PKR Expression and HMGB1 Release Possibly through TLR4/RAGE Receptors High Mobility Group Box Protein 1 (HMGB1): The Prototypical Endogenous Danger Molecule Hematopoietic stem and multipotent progenitor cells produce IL-17, IL-21 and other cytokines in response to TLR signals associated with late apoptotic products and augment memory Th17 and Tc17 cells in the bone marrow of normal and lupus mice HMGB1 mediates anemia of inflammation in murine sepsis survivors.The redox state of the alarmin HMGB1 is a pivotal factor in neuroinflammatory and microglial priming: A role for the NLRP3 inflammasome.HMGB1-Driven Inflammation and Intimal Hyperplasia After Arterial Injury Involves Cell-Specific Actions Mediated by TLR4.Identification of CD163 as an antiinflammatory receptor for HMGB1-haptoglobin complexes.Morphine paradoxically prolongs neuropathic pain in rats by amplifying spinal NLRP3 inflammasome activation B1a cells play a pathogenic role in the development of autoimmune arthritis.Treatment with anti-HMGB1 monoclonal antibody does not affect lupus nephritis in MRL/lpr mice.EGFR mediates hyperlipidemia-induced renal injury via regulating inflammation and oxidative stress: the detrimental role and mechanism of EGFR activation.Blocking Notch signal in myeloid cells alleviates hepatic ischemia reperfusion injury by repressing the activation of NF-κB through CYLD Annexin A5 increases survival in murine sepsis model by inhibiting HMGB1-mediated pro-inflammation and coagulation.HMGB1 Activates Proinflammatory Signaling via TLR5 Leading to Allodynia.Effect of endotoxemia in mice genetically deficient in cystathionine-γ-lyase, cystathionine-β-synthase or 3-mercaptopyruvate sulfurtransferase.Novel strategies for targeting innate immune responses to influenza.Central Role of CD169+ Lymph Node Resident Macrophages in the Adjuvanticity of the QS-21 Component of AS01.The Role of HMGB1 in the Pathogenesis of Type 2 Diabetes.Lupus erythematosus revisited.Recent advances in biomarkers and therapeutic interventions for hepatic drug safety - false dawn or new horizon?Novel perspectives on non-canonical inflammasome activation.HMGB1, IL-1α, IL-33 and S100 proteins: dual-function alarmins Innate Immune Regulations and Liver Ischemia-Reperfusion Injury.HMGB1 is a promising therapeutic target for acute liver failure.The haptoglobin beta subunit sequesters HMGB1 toxicity in sterile and infectious inflammation.Engineering of a self-adjuvanted iTEP-delivered CTL vaccine.Leucine-rich repeat 2 of human Toll-like receptor 4 contains the binding site for inhibitory monoclonal antibodies.Secreted tryptophanyl-tRNA synthetase as a primary defence system against infection.

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MD-2 is required for disulfide HMGB1-dependent TLR4 signaling.

http://www.wikidata.org/entity/Q34924679

description

2015 nî lūn-bûn

@nan

2015 թուականի Յունուարին հրատարակուած գիտական յօդուած

@hyw

2015 թվականի հունվարին հրատարակված գիտական հոդված

@hy

2015年の論文

@ja

2015年論文

@yue

2015年論文

@zh-hant

2015年論文

@zh-hk

2015年論文

@zh-mo

2015年論文

@zh-tw

2015年论文

@wuu

name

MD-2 is required for disulfide HMGB1-dependent TLR4 signaling.

@ast

MD-2 is required for disulfide HMGB1-dependent TLR4 signaling.

@en

MD-2 is required for disulfide HMGB1-dependent TLR4 signaling.

@nl

type

label

MD-2 is required for disulfide HMGB1-dependent TLR4 signaling.

@ast

MD-2 is required for disulfide HMGB1-dependent TLR4 signaling.

@en

MD-2 is required for disulfide HMGB1-dependent TLR4 signaling.

@nl

prefLabel

MD-2 is required for disulfide HMGB1-dependent TLR4 signaling.

@ast

MD-2 is required for disulfide HMGB1-dependent TLR4 signaling.

@en

MD-2 is required for disulfide HMGB1-dependent TLR4 signaling.

@nl

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Journal of Experimental Medicine

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MD-2 is required for disulfide HMGB1-dependent TLR4 signaling.

@en

P2093

Ahmed A Ragab

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

Ben Lu

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

Csaba Szabo

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

Daniel J Antoine

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

Doug T Golenbock

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

Helena E Harris

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

Huan Yang

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

Jesse Roth

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

Jianhua Li

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

Jianmin Meng

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

P2860

Receptor for advanced glycation end products (RAGE)-mediated neurite outgrowth and activation of NF-kappaB require the cytoplasmic domain of the receptor but different downstream signaling pathways

The structural basis of lipopolysaccharide recognition by the TLR4-MD-2 complex

A critical cysteine is required for HMGB1 binding to Toll-like receptor 4 and activation of macrophage cytokine release

Release of chromatin protein HMGB1 by necrotic cells triggers inflammation

HMG-1 as a late mediator of endotoxin lethality in mice

Recombinant HMGB1 with cytokine-stimulating activity

Circulating mitochondrial DAMPs cause inflammatory responses to injury.

MD-2-mediated ionic interactions between lipid A and TLR4 are essential for receptor activation.

The many faces of HMGB1: molecular structure-functional activity in inflammation, apoptosis, and chemotaxis.

Molecular forms of HMGB1 and keratin-18 as mechanistic biomarkers for mode of cell death and prognosis during clinical acetaminophen hepatotoxicity

P304

5-14

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

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scholarly article

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10.1084/JEM.20141318

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P433

1

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

P478

212

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

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Peter Lundbäck

Kevin J. Tracey

Sergio I Valdés-Ferrer

P577

2015-01-05T00:00:00Z

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P5875

273186695

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25559892

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

P921

Toll-like receptor

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4291531

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