Signal transduction by the lipopolysaccharide receptor, Toll-like receptor-4

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Signal transduction by the lipopolysaccharide receptor, Toll-like receptor-4.

An understanding of lipopolysaccharide (LPS) signal transduction is a key goal in the effort to provide a molecular basis for the lethal effect of LPS during septic shock and point the way to novel therapies. Rapid progress in this field during the last 6 years has resulted in the discovery of not only the receptor for LPS - Toll-like receptor 4 (TLR4) - but also in a better appreciation of the...

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Effects of Propofol on Toll-like Receptor 4 Signal Pathway in Alveolar Macrophages Induced by Lipopolysaccharide

Aim: To investigate the effects of propofol on toll-like receptor 4 (TLR4) signaling pathway induced by lipopolysaccharide (LPS) in alveolar macrophages (AMs). Methods: AMs isolated from 10 patients were cultured for 1 hour. These cells were pooled and randomly divided into five groups. The final concentrations of LPS and propofol were 1μg/mL and 30μM, respectively. AMs were continually culture...

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Lipopolysaccharide Induced Activation of Toll Like Receptor 4 in Isolated Rat Heart Suggests a Local Immune Response in Myocardium

Background: Myocardial dysfunction is one of the major complications in patients with sepsis where there is a relationship between the blood level of cytokines and the onset of myocardial depression. In many cases of sepsis, the presence of Lipopolysaccharide (LPS) has been established. LPS Binding Protein (LBP) bound endotoxin is recognized by CD14/toll-like receptor-4 (TLR4) complexes in inna...

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Lysines 128 and 132 enable lipopolysaccharide binding to MD-2, leading to Toll-like receptor-4 aggregation and signal transduction.

Three cell-surface proteins have been recognized as components of the mammalian signaling receptor for bacterial lipopolysaccharide (LPS): CD14, Toll-like receptor-4 (TLR4), and MD-2. Biochemical and visual studies shown here demonstrate that the role of CD14 in signal transduction is to enhance LPS binding to MD-2, although its expression is not essential for cellular activation. These studies...

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ژورنال

عنوان ژورنال: Immunology

سال: 2004

ISSN: 0019-2805,1365-2567

DOI: 10.1111/j.1365-2567.2004.01976.x