SARM inhibits both TRIF- and MyD88-mediated AP-1 activation. - Wikidata - awgldk - TriplyDB

SARM inhibits both TRIF- and MyD88-mediated AP-1 activation.

SARM inhibits both TRIF- and MyD88-mediated AP-1 activation.

http://www.wikidata.org/entity/Q39725027

about

Targeting of pro-apoptotic TLR adaptor SARM to mitochondria: definition of the critical region and residues in the signal sequence UXT plays dual opposing roles on SARM-induced apoptosis Epilepsy and innate immune system: A possible immunogenic predisposition and related therapeutic implications Molecular and cellular regulation of toll-like receptor-4 activity induced by lipopolysaccharide ligands The involvement of cholesterol in sepsis and tolerance to lipopolysaccharide highlighted by the transcriptome analysis of zebrafish (Danio rerio)Litopenaeus vannamei sterile-alpha and armadillo motif containing protein (LvSARM) is involved in regulation of Penaeidins and antilipopolysaccharide factors.TIR domain-containing adaptor SARM is a late addition to the ongoing microbe-host dialog.The innate immunity adaptor SARM translocates to the nucleus to stabilize lamins and prevent DNA fragmentation in response to pro-apoptotic signaling.Activation of TLR3 promotes the degeneration of retinal ganglion cells by upregulating the protein levels of JNK3 Limiting of the innate immune response by SF3A-dependent control of MyD88 alternative mRNA splicing.Molecular characterization of transcriptome-wide interactions between highly pathogenic porcine reproductive and respiratory syndrome virus and porcine alveolar macrophages in vivo.Burkholderia pseudomallei-induced expression of a negative regulator, sterile-alpha and Armadillo motif-containing protein, in mouse macrophages: a possible mechanism for suppression of the MyD88-independent pathway.Characterization of bbtTICAM from amphioxus suggests the emergence of a MyD88-independent pathway in basal chordates Poly(I:C) induces antiviral immune responses in Japanese flounder (Paralichthys olivaceus) that require TLR3 and MDA5 and is negatively regulated by Myd88.Hm-MyD88 and Hm-SARM: two key regulators of the neuroimmune system and neural repair in the medicinal leech Bacillus anthracis TIR Domain-Containing Protein Localises to Cellular Microtubule Structures and Induces Autophagy.Age-dependent changes in innate immune phenotype and function in rhesus macaques (Macaca mulatta).SAM-pointed domain ETS factor mediates epithelial cell-intrinsic innate immune signaling during airway mucous metaplasia T-cell death following immune activation is mediated by mitochondria-localized SARM.SARM1, Not MyD88, Mediates TLR7/TLR9-Induced Apoptosis in Neurons.Activation of the innate signaling molecule MAVS by bunyavirus infection upregulates the adaptor protein SARM1, leading to neuronal death.Excitotoxicity upregulates SARM1 protein expression and promotes Wallerian-like degeneration of retinal ganglion cells and their axons.Resveratrol inhibits the TRIF-dependent pathway by upregulating sterile alpha and armadillo motif protein, contributing to anti-inflammatory effects after respiratory syncytial virus infection.Toll-like receptors are key players in neurodegeneration.Scientific research at Fujian Academy of Integrative Medicine: current status and future directions.The genetics of innate immunity sensors and human disease.Conventional and non-conventional Drosophila Toll signaling.Toll-like receptor 3 in viral pathogenesis: friend or foe?Beyond TLR Signaling—The Role of SARM in Antiviral Immune Defense, Apoptosis & Development.Microbial recognition and danger signals in sepsis and trauma.Reduced Expression of SARM in Mouse Spleen during Polymicrobial Sepsis.Evolution of the TIR domain-containing adaptors in humans: swinging between constraint and adaptation.Oxidative stress and cellular pathways of asthma and inflammation: Therapeutic strategies and pharmacological targets.Innate Immunity in the Persistent Inflammation, Immunosuppression, and Catabolism Syndrome and Its Implications for Therapy.

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P2860

SARM inhibits both TRIF- and MyD88-mediated AP-1 activation.

http://www.wikidata.org/entity/Q39725027

description

2010 nî lūn-bûn

@nan

2010年の論文

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2010年論文

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2010年論文

@zh-hant

2010年論文

@zh-hk

2010年論文

@zh-mo

2010年論文

@zh-tw

2010年论文

@wuu

2010年论文

@zh

2010年论文

@zh-cn

name

SARM inhibits both TRIF- and MyD88-mediated AP-1 activation.

@en

SARM inhibits both TRIF- and MyD88-mediated AP-1 activation.

@nl

type

label

SARM inhibits both TRIF- and MyD88-mediated AP-1 activation.

@en

SARM inhibits both TRIF- and MyD88-mediated AP-1 activation.

@nl

prefLabel

SARM inhibits both TRIF- and MyD88-mediated AP-1 activation.

@en

SARM inhibits both TRIF- and MyD88-mediated AP-1 activation.

@nl

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P1433

European Journal of Immunology

P1476

SARM inhibits both TRIF- and MyD88-mediated AP-1 activation

@en

P2093

Bow Ho

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

Jeak Ling Ding

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

Jun Peng

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

Porkodi Panneerselvam

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

Quan Yuan

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

Soon Kok Lim

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

Xiao Lei Luan

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

Xiaowei Wang

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

P2860

A glycine-rich region in NF-kappaB p105 functions as a processing signal for the generation of the p50 subunit

Lipopolysaccharide-induced expression of matrix metalloproteinases in human monocytes is suppressed by IFN-gamma via superinduction of ATF-3 and suppression of AP-1.

P304

1738-1747

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scholarly article

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10.1002/EJI.200940034

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6

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40

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2010-06-01T00:00:00Z

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42373427

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20306472

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