Tristetraprolin is required for full anti-inflammatory response of murine macrophages to IL-10. - Wikidata - wikimedia - TriplyDB

Tristetraprolin is required for full anti-inflammatory response of murine macrophages to IL-10.

Tristetraprolin is required for full anti-inflammatory response of murine macrophages to IL-10.

http://www.wikidata.org/entity/Q37371476

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Post-transcriptional Regulation of Immunological Responses through Riboclustering Resolution of Inflammation: What Controls Its Onset?The role of macrophages and dendritic cells in the initiation of inflammation in IBD ZFP36L1 negatively regulates erythroid differentiation of CD34+ hematopoietic stem cells by interfering with the Stat5b pathway In vivo actin cross-linking induced by Vibrio cholerae type VI secretion system is associated with intestinal inflammation.Post-transcriptional control during chronic inflammation and cancer: a focus on AU-rich elements.Polyubiquitinated tristetraprolin protects from TNF-induced, caspase-mediated apoptosis HIV-1 gp120 activates the STAT3/interleukin-6 axis in primary human monocyte-derived dendritic cells A noncoding RNA produced by arthropod-borne flaviviruses inhibits the cellular exoribonuclease XRN1 and alters host mRNA stability Suppression of antigen presentation by IL-10 RNase L attenuates mitogen-stimulated gene expression via transcriptional and post-transcriptional mechanisms to limit the proliferative response Tristetraprolin-dependent post-transcriptional regulation of inflammatory cytokine mRNA expression by apolipoprotein A-I: role of ATP-binding membrane cassette transporter A1 and signal transducer and activator of transcription 3.Autophagy activation clears ELAVL1/HuR-mediated accumulation of SQSTM1/p62 during proteasomal inhibition in human retinal pigment epithelial cells Tristetraprolin mediates anti-inflammatory effects of nicotine in lipopolysaccharide-stimulated macrophages.Macrophages make me sick: how macrophage activation states influence sickness behavior Novel phosphorylation-dependent ubiquitination of tristetraprolin by mitogen-activated protein kinase/extracellular signal-regulated kinase kinase kinase 1 (MEKK1) and tumor necrosis factor receptor-associated factor 2 (TRAF2).Tristetraprolin Limits Inflammatory Cytokine Production in Tumor-Associated Macrophages in an mRNA Decay-Independent Manner.Impacts of Salmonella enterica Serovar Typhimurium and Its speG Gene on the Transcriptomes of In Vitro M Cells and Caco-2 Cells.IL-10 regulates Il12b expression via histone deacetylation: implications for intestinal macrophage homeostasis.Cutting edge: IL-10-mediated tristetraprolin induction is part of a feedback loop that controls macrophage STAT3 activation and cytokine production.Differential post-transcriptional regulation of IL-10 by TLR2 and TLR4-activated macrophages Interleukin-10 inhibits lipopolysaccharide-induced tumor necrosis factor-α translation through a SHIP1-dependent pathway.LPS-induced production of TNF-α and IL-6 in mast cells is dependent on p38 but independent of TTP A functional link between heme oxygenase-1 and tristetraprolin in the anti-inflammatory effects of nicotine.Infection-induced IL-10 and JAK-STAT: A review of the molecular circuitry controlling immune hyperactivity in response to pathogenic microbes.Tristetraprolin-driven regulatory circuit controls quality and timing of mRNA decay in inflammation.Tristetraprolin (TTP): interactions with mRNA and proteins, and current thoughts on mechanisms of action.Suppression of IL-12 production by tristetraprolin through blocking NF-kcyB nuclear translocation.Tristetraprolin down-regulates IL-23 expression in colon cancer cells.Apolipoprotein A-I inhibits LPS-induced atherosclerosis in ApoE(-/-) mice possibly via activated STAT3-mediated upregulation of tristetraprolin.Restraint of inflammatory signaling by interdependent strata of negative regulatory pathways The IL-10/STAT3-mediated anti-inflammatory response: recent developments and future challenges.Post-transcriptional coordination of immunological responses by RNA-binding proteins.STAT3 signaling in immunity.Regulation of Interleukin-10 Expression.Post-transcriptional regulation of cytokine and growth factor signaling in cancer.Differences in Tfh Cell Response Between the Graft and Spleen With Chronic Allograft Nephropathy.Casein kinase 2 regulates the mRNA-destabilizing activity of tristetraprolin.Tyrosine kinase 2 controls IL-1ß production at the translational level.A combination of hypoxia and lipopolysaccharide activates tristetraprolin to destabilize proinflammatory mRNAs such as tumor necrosis factor-alpha.

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Tristetraprolin is required for full anti-inflammatory response of murine macrophages to IL-10.

http://www.wikidata.org/entity/Q37371476

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 19 June 2009

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Tristetraprolin is required fo ...... f murine macrophages to IL-10.

@en

Tristetraprolin is required fo ...... f murine macrophages to IL-10.

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type

label

Tristetraprolin is required fo ...... f murine macrophages to IL-10.

@en

Tristetraprolin is required fo ...... f murine macrophages to IL-10.

@nl

prefLabel

Tristetraprolin is required fo ...... f murine macrophages to IL-10.

@en

Tristetraprolin is required fo ...... f murine macrophages to IL-10.

@nl

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JIMMUNOL.0803883

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Journal of Immunology

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Tristetraprolin is required fo ...... f murine macrophages to IL-10.

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Barbara Schaljo

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Claus Vogl

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Franz Kratochvill

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Ines Sauer

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Iwona Sadzak

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Michael Hammer

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Nina Gratz

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Peter J Murray

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

P2860

The tandem CCCH zinc finger protein tristetraprolin and its relevance to cytokine mRNA turnover and arthritis

Evidence that tristetraprolin binds to AU-rich elements and promotes the deadenylation and destabilization of tumor necrosis factor alpha mRNA.

Cytoplasmic localization of tristetraprolin involves 14-3-3-dependent and -independent mechanisms

Cutting edge: A transcriptional repressor and corepressor induced by the STAT3-regulated anti-inflammatory signaling pathway

MK2-induced tristetraprolin:14-3-3 complexes prevent stress granule association and ARE-mRNA decay

MNK1, a new MAP kinase-activated protein kinase, isolated by a novel expression screening method for identifying protein kinase substrates

Feedback inhibition of macrophage tumor necrosis factor-alpha production by tristetraprolin

Stress granules and processing bodies are dynamically linked sites of mRNP remodeling

TTP and BRF proteins nucleate processing body formation to silence mRNAs with AU-rich elements

Involvement of microRNA in AU-rich element-mediated mRNA instability

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1197-1206

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scholarly article

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10.4049/JIMMUNOL.0803883

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2

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183

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Mathias Müller

Perry J. Blackshear

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2009-06-19T00:00:00Z

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26307110

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19542371

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2755621

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