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Human Toll-like receptor 2 confers responsiveness to bacterial lipopolysaccharide

by J. Kirschning, Holger Wesche, T. Merrill Ayres, Mike Rothe , 1998
"... Bacterial lipopolysaccharide (LPS) induces activation of the transcription factor nuclear factor �B (NF-�B) in host cells upon infection. LPS binds to the glycosylphosphatidylinositol (GPI)anchored membrane protein CD14, which lacks an intracellular signaling domain. Here we investigated the role of ..."
Abstract - Cited by 99 (4 self) - Add to MetaCart
through TLR2 was dependent on serum which contains soluble CD14 (sCD14). Coexpression of CD14 synergistically enhanced LPS signal transmission through TLR2. In addition, purified recombinant sCD14 could substitute for serum to support LPS-induced TLR2 activation. LPS stimulation of TLR2 initiated

MD-2 as the Target of Nonlipid Chalcone in the Inhibition of Endotoxin LPS-Induced TLR4 Activity

by Nam Doo Kim, Sang-bae Han, Youngsoo Kim
"... Myeloid differentiation 2 (MD-2) recognizes endotoxin lipopolysaccharide (LPS), which is required for Toll-like receptor 4 (TLR4) activity. MD-2 represents a more attractive therapeutic target than TLR4 for intervention in severe inflammatory disorders due to microbial infection. Here, we suggest MD ..."
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Myeloid differentiation 2 (MD-2) recognizes endotoxin lipopolysaccharide (LPS), which is required for Toll-like receptor 4 (TLR4) activity. MD-2 represents a more attractive therapeutic target than TLR4 for intervention in severe inflammatory disorders due to microbial infection. Here, we suggest

Stamme C. Surfactant protein-A modulates LPS-induced TLR4 localization and signaling via β-arrestin 2

by Vicky Sender - PLoS One 2013; 8:e59896; PMID:23536892; http://dx.doi.org/10.1371/journal.pone.0059896
"... The soluble C-type lectin surfactant protein (SP)-A mediates lung immune responses partially via its direct effects on alveolar macrophages (AM), the main resident leukocytes exposed to antigens. SP-A modulates the AM threshold of lipopolysaccharide (LPS) activity towards an anti-inflammatory phenot ..."
Abstract - Cited by 2 (0 self) - Add to MetaCart
-inflammatory phenotype both in vitro and in vivo through various mechanisms. LPS responses are tightly regulated via distinct pathways including subcellular TLR4 localization and thus ligand sensing. The cytosolic scaffold and signaling protein b-arrestin 2 acts as negative regulator of LPS-induced TLR4 activation. Here

REVIEW Co-operation of TLR4 and raft proteins in LPS-induced pro-inflammatory signaling

by Aneta Hromada-judycka, Katarzyna Kwiatkowska
"... Abstract Toll-like receptor 4 (TLR4) is activated by lipopolysaccharide (LPS), a component of Gram-negative bacteria to induce production of pro-inflammatory media-tors aiming at eradication of the bacteria. Dysregulation of the host responses to LPS can lead to a systemic inflam-matory condition na ..."
Abstract - Cited by 1 (0 self) - Add to MetaCart
Abstract Toll-like receptor 4 (TLR4) is activated by lipopolysaccharide (LPS), a component of Gram-negative bacteria to induce production of pro-inflammatory media-tors aiming at eradication of the bacteria. Dysregulation of the host responses to LPS can lead to a systemic inflam-matory condition

The Transcription Factor C/EBP-b Mediates Constitutive and LPS-Inducible Transcription of Murine SerpinB2

by Ekemini A. Udofa, Brett W. Stringer, Padmaja Gade, Donna Mahony, Marguerite S. Buzza, Dhananjaya V. Kalvakolanu, Toni M. Antalis
"... SerpinB2 or plasminogen activator inhibitor type 2 (PAI-2) is highly induced in macrophages in response to inflammatory stimuli and is linked to the modulation of innate immunity, macrophage survival, and inhibition of plasminogen activators. Lipopolysaccharide (LPS), a potent bacterial endotoxin, c ..."
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. Mutation analyses revealed that a CCAAT enhancer binding (C/EBP) element, a cyclic AMP response element (CRE) and two activator protein 1 (AP-1) response elements in the murine SerpinB2 proximal promoter are essential for optimal LPS-inducibility. Electrophoretic mobility shift (EMSA) and chromatin

Simvastatin suppresses LPS-induced MMP-1 expression in

by John J. S, Maria F. Lopes-virella, Yan Huang
"... U937 mononuclear cells by inhibiting protein isoprenylation-mediated ERK activation ..."
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U937 mononuclear cells by inhibiting protein isoprenylation-mediated ERK activation

Intermedin Attenuates LPS-induced Inflammation in the Rat Testis

by Lei Li, Ping Ma, Yongjun Liu, Chen Huang, Wai-sum O, Fai Tang, Jian V. Zhang
"... First reported as a vasoactive peptide in the cardiovascular system, intermedin (IMD), also known as adrenomedullin 2 (ADM2), is a hormone with multiple potent roles, including its antioxidant action on the pulmonary, central nervous, cardiovascular and renal systems. Though IMD may play certain rol ..."
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in the testes. In a rat model, bacterial lippolysaccharide (LPS) induced atypical orchitis, and LPS treatment upregulated the expression of IMD and one of its receptor component proteins, i.e. receptor activity modifying protein 2 (RAMP2). IMD decreased both plasma and testicular levels of reactive oxygen

Research Article Amelioration of LPS-Induced Inflammation Response

by Microglia Ampk Activation
"... Copyright © 2014 Chin-Chen Chen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Adenosine 5-monophosphate-activated protein ki ..."
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Copyright © 2014 Chin-Chen Chen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Adenosine 5-monophosphate-activated protein

Surfactant protein A inhibits lipopolysaccharide (LPS)-induced immune cell activation by preventing the interaction of LPS with LPS-binding protein

by Cordula Stamme, Mareike Müller, Lutz Hamann, Thomas Gutsmann, Ulrich Seydel - Am. J. Respir. Cell Mol. Biol , 2002
"... Pulmonary surfactant protein (SP)-A, an innate immune molecule, modifies lipopolysaccharide (LPS)-induced cell responses. Because SP-A avidly binds to the deep rough (Re) mutant of LPS, we first investigated the functional consequences of this interaction and found that preincubation of Re-LPS with ..."
Abstract - Cited by 9 (3 self) - Add to MetaCart
activation was abrogated. Because LBP-catalyzed binding of LPS to CD14 is essential for low-dose LPS-induced signaling, we then hypothesized that SP-A inhibits Re-LPS–induced immune cell activation via inhibiting the binding of Re-LPS to LBP. Binding competition experiments employing a surface plasmon

Pre-Treatment of Recombinant Mouse MFG-E8 Downregulates LPS-Induced TNF-a Production in Macrophages via STAT3-Mediated SOCS3 Activation

by Monowar Aziz, Asha Jacob, Akihisa Matsuda, Rongqian Wu, Mian Zhou, Weifeng Dong, Weng-lang Yang, Ping Wang
"... Milk fat globule-epidermal growth factor factor 8 (MFG-E8) regulates innate immune function by modulating cellular signaling, which is less understood. Herein, we aimed to investigate the direct anti-inflammatory role of MFG-E8 in macrophages by pre-treatment with recombinant murine MFG-E8 (rmMFG-E8 ..."
Abstract - Cited by 4 (1 self) - Add to MetaCart
MFG-E8) followed by stimulation with LPS in RAW264.7 cells and in peritoneal macrophages, isolated from wild-type (WT) or MFG-E8 2/2 mice. RAW264.7 cells and mouse peritoneal macrophages treated with rmMFG-E8 significantly downregulated LPS-induced TNF-a mRNA by 25% and 24%, and protein levels by 29
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