Glucocorticoids suppress inflammation via the upregulation of negative regulator IRAK-M. - Test2 - elhamkhani - TriplyDB

Glucocorticoids suppress inflammation via the upregulation of negative regulator IRAK-M.

Glucocorticoids suppress inflammation via the upregulation of negative regulator IRAK-M.

http://www.wikidata.org/entity/Q35023017

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Gene Expression Control by Glucocorticoid Receptors during Innate Immune Responses Glucocorticoid-independent modulation of GR activity: Implications for immunotherapy BCL-2 protects human and mouse Th17 cells from glucocorticoid-induced apoptosis Bifunctional Conjugates with Potent Inhibitory Activity Towards Cyclooxygenase and Histone Deacetylase Nontypeable Haemophilus influenzae-Induced MyD88 Short Expression Is Regulated by Positive IKKβ and CREB Pathways and Negative ERK1/2 Pathway.The role of Interleukin Receptor Associated Kinase (IRAK)-M in regulation of myofibroblast phenotype in vitro, and in an experimental model of non-reperfused myocardial infarction.Endogenous hepatic glucocorticoid receptor signaling coordinates sex-biased inflammatory gene expression.Deubiquitinase CYLD acts as a negative regulator for bacterium NTHi-induced inflammation by suppressing K63-linked ubiquitination of MyD88.Socs1 and Socs3 degrades Traf6 via polyubiquitination in LPS-induced acute necrotizing pancreatitis.Cistrome-based Cooperation between Airway Epithelial Glucocorticoid Receptor and NF-κB Orchestrates Anti-inflammatory Effects Resveratrol suppresses NTHi-induced inflammation via up-regulation of the negative regulator MyD88 short.An inhaled dose of budesonide induces genes involved in transcription and signaling in the human airways: enhancement of anti- and proinflammatory effector genes.Nucleotide-binding mechanisms in pseudokinases.Glucocorticoid receptors: finding the middle ground.Preconditioning with recombinant high-mobility group box 1 induces ischemic tolerance in a rat model of focal cerebral ischemia-reperfusion.A structure-activity relationship of non-peptide macrocyclic histone deacetylase inhibitors and their anti-proliferative and anti-inflammatory activities.Genome Expression Profiling-Based Identification and Administration Efficacy of Host-Directed Antimicrobial Drugs against Respiratory Infection by Nontypeable Haemophilus influenzae.Understanding how long-acting β2 -adrenoceptor agonists enhance the clinical efficacy of inhaled corticosteroids in asthma - an update.Glucocorticoid and cytokine crosstalk: Feedback, feedforward, and co-regulatory interactions determine repression or resistance.Limiting inflammation-the negative regulation of NF-κB and the NLRP3 inflammasome.Glucocorticoid and TNF signaling converge at A20 (TNFAIP3) to repress airway smooth muscle cytokine expression Antimicrobial Peptide Epinecidin-1 Modulates MyD88 Protein Levels via the Proteasome Degradation Pathway.Protective effect of dexamethasone on 5-FU-induced oral mucositis in hamsters.Critical Role of IRAK-M in Regulating Antigen-Induced Airway Inflammation.Long-acting β2-agonists promote glucocorticoid-mediated repression of NF-κB by enhancing expression of the feedback regulator TNFAIP3.

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Glucocorticoids suppress inflammation via the upregulation of negative regulator IRAK-M.

http://www.wikidata.org/entity/Q35023017

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2015 nî lūn-bûn

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2015 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2015 թվականի հունվարին հրատարակված գիտական հոդված

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2015年の論文

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2015年論文

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2015年論文

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2015年論文

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2015年論文

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2015年論文

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2015年论文

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name

Glucocorticoids suppress inflammation via the upregulation of negative regulator IRAK-M.

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Glucocorticoids suppress inflammation via the upregulation of negative regulator IRAK-M.

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type

label

Glucocorticoids suppress inflammation via the upregulation of negative regulator IRAK-M.

@ast

Glucocorticoids suppress inflammation via the upregulation of negative regulator IRAK-M.

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prefLabel

Glucocorticoids suppress inflammation via the upregulation of negative regulator IRAK-M.

@ast

Glucocorticoids suppress inflammation via the upregulation of negative regulator IRAK-M.

@en

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Nature Communications

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Glucocorticoids suppress inflammation via the upregulation of negative regulator IRAK-M.

@en

P2093

Haidong Xu

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Hirofumi Kai

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Ji-Yun Lee

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Jian-Dong Li

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Koichi S Kobayashi

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Masanori Miyata

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Seiko Susuki-Miyata

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Wenzhuo Y Wang

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P2860

IRAK-M is a novel member of the Pelle/interleukin-1 receptor-associated kinase (IRAK) family

Differential regulation and role of interleukin-1 receptor associated kinase-M in innate immunity signaling

IRAK-M is a negative regulator of Toll-like receptor signaling

The NF-kappa B and I kappa B proteins: new discoveries and insights

IKK-1 and IKK-2: cytokine-activated IkappaB kinases essential for NF-kappaB activation

The glucocorticoid receptor inhibits NFkappaB by interfering with serine-2 phosphorylation of the RNA polymerase II carboxy-terminal domain

Pyogenic bacterial infections in humans with MyD88 deficiency

IRAK-M is involved in the pathogenesis of early-onset persistent asthma

Glucocorticoid receptor signaling in health and disease

Disease tolerance as a defense strategy

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10.1038/NCOMMS7062

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6

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Richard Flavell

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