Genetic Deletion of the Tumor Necrosis Factor Receptor p60 or p80 Sensitizes Macrophages to Lipopolysaccharide-induced Nuclear Factor-κB, Mitogen-activated Protein Kinases, and Apoptosis
Open Access
- 1 June 2003
- journal article
- Published by Elsevier BV
- Vol. 278 (26), 23390-23397
- https://doi.org/10.1074/jbc.m213237200
Abstract
No abstract availableKeywords
This publication has 56 references indexed in Scilit:
- Modulation of the expression of cyclooxygenase‐2 by fatty acids mediated through Toll‐like receptor 4‐derived signaling pathways1The FASEB Journal, 2001
- Genetic Deletion of the Tumor Necrosis Factor Receptor p60 or p80 Abrogates Ligand-mediated Activation of Nuclear Factor-κB and of Mitogen-activated Protein Kinases in MacrophagesJournal of Biological Chemistry, 2001
- Cellular Events Mediated by Lipopolysaccharide-stimulated Toll-like Receptor 4Published by Elsevier BV ,2000
- Differential Effects of Lipopolysaccharide and Tumor Necrosis Factor on Monocytic IκB Kinase Signalsome Activation and IκB ProteolysisPublished by Elsevier BV ,1999
- Endotoxin-tolerant Mice Have Mutations in Toll-like Receptor 4 (Tlr4)The Journal of Experimental Medicine, 1999
- Resistance to Endotoxin Shock and Reduced Dissemination of Gram-Negative Bacteria in CD14-Deficient MiceImmunity, 1996
- TNF-Dependent Recruitment of the Protein Kinase RIP to the TNF Receptor-1 Signaling ComplexImmunity, 1996
- Does endotoxin stimulate cells by mimicking ceramide?Immunology Today, 1995
- A MAP Kinase Targeted by Endotoxin and Hyperosmolarity in Mammalian CellsScience, 1994
- CD14, a Receptor for Complexes of Lipopolysaccharide (LPS) and LPS Binding ProteinScience, 1990