Epidermal loss of JunB leads to a SLE phenotype due to hyper IL-6 signaling. - Wikidata - awgldk - TriplyDB

Epidermal loss of JunB leads to a SLE phenotype due to hyper IL-6 signaling.

Epidermal loss of JunB leads to a SLE phenotype due to hyper IL-6 signaling.

http://www.wikidata.org/entity/Q37453484

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Applications of systems approaches in the study of rheumatic diseases.Effects of the loss of conjunctival Muc16 on corneal epithelium and stroma in mice Junb controls lymphatic vascular development in zebrafish via miR-182.Stat3 promotes IL-10 expression in lupus T cells through trans-activation and chromatin remodeling Platelet-activating factor blockade inhibits the T-helper type 17 cell pathway and suppresses psoriasis-like skin disease in K5.hTGF-β1 transgenic mice.Specific roles for dendritic cell subsets during initiation and progression of psoriasis.Candidate gene identification for systemic lupus erythematosus using network centrality measures and gene ontology.AP-1 transcription factor JunD confers protection from accelerated nephrotoxic nephritis and control podocyte-specific Vegfa expression.IL-6 promotes acute and chronic inflammatory disease in the absence of SOCS3.Cytokine disturbances in systemic lupus erythematosus.Genetic disruption of Fra-1 decreases susceptibility to endotoxin-induced acute lung injury and mortality in mice Tocilizumab for the treatment of rheumatoid arthritis and other systemic autoimmune diseases: current perspectives and future directions.Roles of pro- and anti-inflammatory cytokines in the pathogenesis of SLE Differential Expression of the Activator Protein 1 Transcription Factor Regulates Interleukin-1ß Induction of Interleukin 6 in the Developing Enterocyte.Phylotype-level 16S rRNA analysis reveals new bacterial indicators of health state in acute murine colitis.The transcription factors Egr2 and Egr3 are essential for the control of inflammation and antigen-induced proliferation of B and T cells.Intestinal Microbiota Signatures Associated with Inflammation History in Mice Experiencing Recurring Colitis.Cytokines and their roles in the pathogenesis of systemic lupus erythematosus: from basics to recent advances.Immunotherapeutic implication of IL-6 blockade.Targeting interleukin-6: all the way to treat autoimmune and inflammatory diseases.SOCS signaling in autoimmune diseases: molecular mechanisms and therapeutic implications.Chronic systemic inflammation originating from epithelial tissues.PDGFR blockade is a rational and effective therapy for NPM-ALK-driven lymphomas.Chronic skin inflammation leads to bone loss by IL-17-mediated inhibition of Wnt signaling in osteoblasts.Desired response to phototherapy vs photoaggravation in psoriasis: what makes the difference?Mast cells are required for phototolerance induction and scratching abatement.AP1 transcription factors in epidermal differentiation and skin cancer Interleukin-6 receptor alpha blockade improves skin lesions in a murine model of systemic lupus erythematosus.The new era of autoimmune disease research.Phototherapeutic hardening modulates systemic cytokine levels in patients with polymorphic light eruption.Lupus Skin Is Primed for IL-6 Inflammatory Responses through a Keratinocyte-Mediated Autocrine Type I Interferon Loop.Dysregulation of the suppressor of cytokine signalling 3-signal transducer and activator of transcription-3 pathway in the aetiopathogenesis of Sjögren's syndrome.Photohardening restores the impaired neutrophil responsiveness to chemoattractants leukotriene B4 and formyl-methionyl-leucyl-phenylalanin in patients with polymorphic light eruption Pancreatic β-cells activate a JunB/ATF3-dependent survival pathway during inflammation JunB defines functional and structural integrity of the epidermo-pilosebaceous unit in the skin

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P2860

Epidermal loss of JunB leads to a SLE phenotype due to hyper IL-6 signaling.

http://www.wikidata.org/entity/Q37453484

description

2009 nî lūn-bûn

@nan

2009年の論文

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2009年学术文章

@wuu

2009年学术文章

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2009年学术文章

@zh-hans

2009年学术文章

@zh-my

2009年学术文章

@zh-sg

2009年學術文章

@yue

2009年學術文章

@zh

2009年學術文章

@zh-hant

name

Epidermal loss of JunB leads to a SLE phenotype due to hyper IL-6 signaling.

@en

Epidermal loss of JunB leads to a SLE phenotype due to hyper IL-6 signaling.

@nl

type

label

Epidermal loss of JunB leads to a SLE phenotype due to hyper IL-6 signaling.

@en

Epidermal loss of JunB leads to a SLE phenotype due to hyper IL-6 signaling.

@nl

prefLabel

Epidermal loss of JunB leads to a SLE phenotype due to hyper IL-6 signaling.

@en

Epidermal loss of JunB leads to a SLE phenotype due to hyper IL-6 signaling.

@nl

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PNAS.0910371106

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Proceedings of the National Academy of Sciences of the United States of America

P1476

Epidermal loss of JunB leads to a SLE phenotype due to hyper IL-6 signaling

@en

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Afschin Soleiman

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

Arabella Meixner

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

Brigitte Hantusch

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Elke Janig

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Michaela Schlederer

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

Pamina Pflegerl

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Paul Vesely

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

Peter Wolf

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

Rainer Zenz

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

Tadamitsu Kishimoto

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

P2860

Principles of interleukin (IL)-6-type cytokine signalling and its regulation

Basic local alignment search tool

AP-1: a double-edged sword in tumorigenesis

Mechanisms of autoantibody diversification to SLE-related autoantigens.

Anticytokine therapy in autoimmune diseases.

IgG1 plasmacytosis in interleukin 6 transgenic mice.

Psoriasis-like skin disease and arthritis caused by inducible epidermal deletion of Jun proteins.

The paradigm of IL-6: from basic science to medicine

Specific antinuclear antibodies are associated with clinical features in systemic lupus erythematosus

Interleukin-6 exacerbates glomerulonephritis in (NZB x NZW)F1 mice.

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20423-20428

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10.1073/PNAS.0910371106

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48

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106

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Richard Moriggl

Peter Petzelbauer

Guenter Steiner

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2009-11-16T00:00:00Z

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38093892

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19918056

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2787143

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