IRAK-1 Contributes to Lipopolysaccharide-induced Reactive Oxygen Species Generation in Macrophages by Inducing NOX-1 Transcription and Rac1 Activation and Suppressing the Expression of Antioxidative Enzymes-Reference-Cited by-同舟云学术

IRAK-1 Contributes to Lipopolysaccharide-induced Reactive Oxygen Species Generation in Macrophages by Inducing NOX-1 Transcription and Rac1 Activation and Suppressing the Expression of Antioxidative Enzymes

Published:2009-12 Issue:51 Volume:284 Page:35403-35411
ISSN:0021-9258
Container-title:Journal of Biological Chemistry
language:en
Short-container-title:Journal of Biological Chemistry

Author:

Maitra Urmila,Singh Neeraj,Gan Lu,Ringwood Lorna,Li Liwu

Publisher

Elsevier BV

Subject

Cell Biology,Molecular Biology,Biochemistry

Reference41 articles.

1. Endotoxin-Induced Mortality Is Related to Increased Oxidative Stress and End-Organ Dysfunction, Not Refractory Hypotension, in Heme Oxygenase-1–Deficient Mice

2. Impaired Priming and Activation of the Neutrophil NADPH Oxidase in Patients with IRAK4 or NEMO Deficiency

3. Regulation of the phagocyte NADPH oxidase activity: phosphorylation of gp91phox/NOX2 by protein kinase C enhances its diaphorase activity and binding to Rac2, p67phox, and p47phox

4. Interactive role of the toll-like receptor 4 and reactive oxygen species in LPS-induced microglia activation

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