The DOI matches its Crossref record; 30 of the 30 references it cites were found in a registry or an index.
Rip1 Mediates the Trif-dependent Toll-like Receptor 3- and 4-induced NF-κB Activation but Does Not Contribute to Interferon Regulatory Factor 3 Activation
Open accessAbstract
Rip1 is required for IkappaB kinase activation in response to tumor necrosis factor alpha (TNF-alpha) and has been implicated in the Toll-like receptor 3 (TLR3) response to double-stranded RNA. Cytokine production is impaired when rip1-/- cells are treated with TNF-alpha, poly(I-C), or lipopolysaccharide, implicating Rip1 in the Trif-dependent TLR3 and TLR4 pathways. To examine the role of Rip1 in the Trif-dependent TLR4 pathway, we generated rip1-/- MyD88-/- cells. Lipopolysaccharide failed to stimulate NF-kappaB activation in rip1-/-MyD88-/- cells, revealing that Rip1 is also required for the Trif-dependent TLR4-induced NF-kappaB pathway. In addition to activating NF-kappaB, TLR3/4 pathways also stimulate interferon regulatory factor 3 activation. However, we find that Rip1 expression stimulates NF-kappaB but not interferon regulatory factor 3 activity. In the TNF-alpha pathway, Rip1 interacts with the E3 ubiquitin ligase Traf2 and is modified by polyubiquitin chains. Upon TLR3 activation, Rip1 is also modified by polyubiquitin chains and is recruited to TLR3 along with Traf6 and the ubiquitin-activated kinase Tak1. These studies suggest that Rip1 uses a similar, ubiquitin-dependent mechanism to activate IkappaB kinase-beta in response to TNF-alpha and TLR3 ligands.
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Role of Adaptor TRIF in the MyD88-Independent Toll-Like Receptor Signaling Pathway
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IKKε and TBK1 are essential components of the IRF3 signaling pathway
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Self-citationUnresponsiveness of MyD88-Deficient Mice to Endotoxin
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De-ubiquitination and ubiquitin ligase domains of A20 downregulate NF-κB signalling
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TNF-Dependent Recruitment of the Protein Kinase RIP to the TNF Receptor-1 Signaling Complex
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The Death Domain Kinase RIP Mediates the TNF-Induced NF-κB Signal
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Self-citationThe ubiquitin-modifying enzyme A20 is required for termination of Toll-like receptor responses
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Cited by
Shared Principles in NF-κB Signaling
Hayden, M. S., & Ghosh, S. (2008) · Cell · doi:10.1016/j.cell.2008.01.020 · Cited by 4,494
LPS/TLR4 signal transduction pathway
Lu, Y.-C., Yeh, W.-C., & Ohashi, P. S. (2008) · Cytokine · doi:10.1016/j.cyto.2008.01.006 · Cited by 3,301
Pathogen Recognition and Inflammatory Signaling in Innate Immune Defenses
Mogensen, T. H. (2009) · Clinical Microbiology Reviews · doi:10.1128/cmr.00046-08 · Cited by 3,111
The family of five: TIR-domain-containing adaptors in Toll-like receptor signalling
O'Neill, L. A. J., & Bowie, A. G. (2007) · Nature Reviews Immunology · doi:10.1038/nri2079 · Cited by 2,667
Cho, Y., Challa, S., Moquin, D., Genga, R., Ray, T. D., Guildford, M., & Chan, F. K.-M. (2009) · Cell · doi:10.1016/j.cell.2009.05.037 · Cited by 2,435
Metadata
- Authors
- Cusson-Hermance, N., Khurana, S., Lee, T. H., Fitzgerald, K. A., & Kelliher, M. A.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2005-11
- Volume
- 280
- Issue
- 44
- Pages
- 36560-36566
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2146739467
- Cited by
- 344
- References
- 30
- FWCI
- 7.40
- Type
- journal article
- Language
- en
- Open access
- hybrid
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- creativecommons.org/licenses/by/4.0/ (vor, 5449 d)
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- The paper
- Cusson-Hermance, N., Khurana, S., Lee, T. H., Fitzgerald, K. A., & Kelliher, M. A. (2005). Rip1 Mediates the Trif-dependent Toll-like Receptor 3- and 4-induced NF-κB Activation but Does Not Contribute to Interferon Regulatory Factor 3 Activation. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.m506831200
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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