Epidermal loss of JunB leads to a SLE phenotype due to hyper IL-6 signaling.
about
Applications of systems approaches in the study of rheumatic diseases.Effects of the loss of conjunctival Muc16 on corneal epithelium and stroma in miceJunb controls lymphatic vascular development in zebrafish via miR-182.Stat3 promotes IL-10 expression in lupus T cells through trans-activation and chromatin remodelingPlatelet-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 miceTocilizumab 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 SLEDifferential 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 cancerInterleukin-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 eruptionPancreatic β-cells activate a JunB/ATF3-dependent survival pathway during inflammationJunB defines functional and structural integrity of the epidermo-pilosebaceous unit in the skin
P2860
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P2860
Epidermal loss of JunB leads to a SLE phenotype due to hyper IL-6 signaling.
description
2009 nî lūn-bûn
@nan
2009年の論文
@ja
2009年学术文章
@wuu
2009年学术文章
@zh-cn
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
P2093
P2860
P50
P356
P1476
Epidermal loss of JunB leads to a SLE phenotype due to hyper IL-6 signaling
@en
P2093
Afschin Soleiman
Arabella Meixner
Brigitte Hantusch
Elke Janig
Michaela Schlederer
Pamina Pflegerl
Paul Vesely
Peter Wolf
Rainer Zenz
Tadamitsu Kishimoto
P2860
P304
20423-20428
P356
10.1073/PNAS.0910371106
P407
P577
2009-11-16T00:00:00Z