A TLR4/MD2 fusion protein inhibits LPS-induced pro-inflammatory signaling in hepatic stellate cells

Schnabl, Bernd; Brandl, Katharina; Fink, Marina; Groß, Philipp; Taura, Kojiro; Gäbele, Erwin; Hellerbrand, Claus; Falk, Werner

doi:10.1016/j.bbrc.2008.07.150

Cited by 35 publications

(28 citation statements)

References 26 publications

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“…Cell sensitivity to LPS is likely to be controlled by the modulation of TLR4 biosynthesis or activity through changes in sensitivities to the signals initiated or received by TLR4. It is well confirmed that blocking MD-2 or TLR4/MD-2 by antagonists may help to attenuate the severity of inflammation induced by LPS-activated AMs [10][11][12][13]. Taken together, MD-2 is an interesting and logical target for pharmacological intervention to prevent or attenuate excessive lung inflammation.…”

Section: Introductionmentioning

confidence: 87%

Myeloid differentiation protein 2 silencing decreases LPS-induced cytokine production and TLR4/MyD88 pathway activity in alveolar macrophages

Ren

Feng

et al. 2011

Immunology Letters

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Section: Introductionmentioning

confidence: 87%

Myeloid differentiation protein 2 silencing decreases LPS-induced cytokine production and TLR4/MyD88 pathway activity in alveolar macrophages

Ren

Feng

et al. 2011

Immunology Letters

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“…The secretion of cytokines and chemokines, including TNFa, IL6, IL1b, MIP-1a, MIP-1b, and RANTES by HSCs is regulated by a variety of cell surface receptors, including pattern recognition receptors such as Toll-like receptors (TLRs). Activation of TLR-4 by lipopolysaccharide (LPS) stimulates synthesis of interferon-c, TNFa, IL6 and IL1b by both quiescent and activated HSCs [11][12][13].…”

Section: Introductionmentioning

confidence: 99%

SHP-dependent and -independent induction of peroxisome proliferator-activated receptor-γ by the bile acid sensor farnesoid X receptor counter-regulates the pro-inflammatory phenotype of liver myofibroblasts

et al. 2011

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“…LY96's molecular function consists of miscellaneous function and transmembrane receptor regulatory/adaptor protein, and it is concerned with biological process of immunity and defense (DAVID). LY96's relational study also can be presented in these articles [42][43][44][45][46].…”

Section: Discussionmentioning

confidence: 99%

CREB5 Computational Regulation Network Construction and Analysis Between Frontal Cortex of HIV Encephalitis (HIVE) and HIVE-Control Patients

Wang

Huang

Jiang

2010

Cell Biochem Biophys

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CREB5 computational regulation network construction and analysis of frontal cortex of HIV encephalitis (HIVE) is very useful to identify novel markers and potential targets for prognosis and therapy. By integration of gene regulatory network infer and the database for annotation, visualization and integrated discovery we identified and constructed significant molecule CREB5 regulation network from 12 frontal cortex of HIVE-control patients and 16 HIVE in the same GEO Dataset GDS1726. Our result verified CREB5 biological regulation module in the upstream of frontal cortex of HIVE-control patients (MAPKAPK3 activation; DGKG, LY96, TNFRSF11B inhibition) and downstream (ATP6V0E1, CFB, DGKG, MX1, TGFBR3 activation; LGALS3BP, RASGRP3, RDX, STAT1 inhibition), whereas in the upstream of frontal cortex of HIVE (BST2, CFB, LCAT, TNFRSF11B activation; CFHR1, LY96 inhibition) and downstream (GAS1, LCAT, LGALS3BP, NFAT5, VEZF1, ZNF652 activation; DGKG, IFITM1, LY96, TNFRSF11B inhibition). Importantly, we datamined that CREB5 regulation cluster of HIVE was involved in inflammatory response, proteolysis, biological adhesion, and negative regulation of biological process (only in HIVE terms) without positive regulation of cellular process, phosphotransferase, kinase, post-translational protein modification, ATP binding, transmembrane protein, calcium ion binding, acetylation, and hydrolase activity (only in HIVE-control patients terms), the condition was vital to inflammation and cognition impairment of HIVE. Our result demonstrated that common terms in both HIVE-control patients and HIVE included biological regulation, phosphoprotein, metabolic process, zinc, biosynthetic process, organelle, signal transduction, defense response, membrane, secreted, signal peptide, and glycoprotein, and these terms were more relative to inflammation and cognition impairment, therefore we deduced the stronger CREB5 regulation network in HIVE consistent with our number computation. It would be necessary of the stronger CREB5 regulation function to inflammation and cognition impairment of HIVE.

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A TLR4/MD2 fusion protein inhibits LPS-induced pro-inflammatory signaling in hepatic stellate cells

Cited by 35 publications

References 26 publications

Myeloid differentiation protein 2 silencing decreases LPS-induced cytokine production and TLR4/MyD88 pathway activity in alveolar macrophages

Myeloid differentiation protein 2 silencing decreases LPS-induced cytokine production and TLR4/MyD88 pathway activity in alveolar macrophages

SHP-dependent and -independent induction of peroxisome proliferator-activated receptor-γ by the bile acid sensor farnesoid X receptor counter-regulates the pro-inflammatory phenotype of liver myofibroblasts

CREB5 Computational Regulation Network Construction and Analysis Between Frontal Cortex of HIV Encephalitis (HIVE) and HIVE-Control Patients

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