Myeloid depletion of SOCS3 enhances LPS-induced acute lung injury through CCAAT/enhancer binding protein δ pathway
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Title
Myeloid depletion of SOCS3 enhances LPS-induced acute lung injury through CCAAT/enhancer binding protein δ pathway
Authors
Keywords
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Journal
FASEB JOURNAL
Volume 27, Issue 8, Pages 2967-2976
Publisher
FASEB
Online
2013-04-13
DOI
10.1096/fj.12-225797
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Note: Only part of the references are listed.- CCAAT/Enhancer-Binding Protein δ Is a Critical Mediator of Lipopolysaccharide-Induced Acute Lung Injury
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- Inhibiting Mer receptor tyrosine kinase suppresses STAT1, SOCS1/3, and NF-κB activation and enhances inflammatory responses in lipopolysaccharide-induced acute lung injury
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- Resolution of Toll-like receptor 4-mediated acute lung injury is linked to eicosanoids and suppressor of cytokine signaling 3
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- Suppressor of Cytokine Signaling 3 Inhibits LPS-induced IL-6 Expression in Osteoblasts by Suppressing CCAAT/Enhancer-binding Protein β Activity
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- Recent trends in acute lung injury mortality: 1996–2005*
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- Acute Lung Injury:Apoptosis and Signaling Mechanisms
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- Differential Role for c-Rel and C/EBP / in TLR-Mediated Induction of Proinflammatory Cytokines
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- Splenic suppressor of cytokine signaling 3 transgene expression affects T cell responses and prevents development of collagen-induced arthritis
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- SOCS3 promotes TLR4 response in macrophages by feedback inhibiting TGF-β1/Smad3 signaling
- (2007) Xia Liu et al. MOLECULAR IMMUNOLOGY
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