ECSIT is an evolutionarily conserved intermediate in the Toll/IL-1 signal transduction pathway
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Activation of NF-kappaB as a consequence of signaling through the Toll and IL-1 receptors is a major element of innate immune responses. We report the identification and characterization of a novel intermediate in these signaling pathways that bridges TRAF6 to MEKK-1. This adapter protein, which we have named ECSIT (evolutionarily conserved signaling intermediate in Toll pathways), is specific for the Toll/IL-1 pathways and is a regulator of MEKK-1 processing. Expression of wild-type ECSIT accelerates processing of MEKK-1, whereas a dominant-negative fragment of ECSIT blocks MEKK-1 processing and activation of NF-kappaB. These results indicate an important role for ECSIT in signaling to NF-kappaB and suggest that processing of MEKK-1 is required for its function in the Toll/IL-1 pathway.
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Internal initiation in the signaling scaffold Ecsit produces a protein nearly identical to a dominant negative form created by designed N-terminal deletion.
“internal initiation in the signaling scaffold Ecsit produces a protein nearly identical to a dominant negative form created by designed N-terminal deletion”
From Ribosome Profiling of Mouse Embryonic Stem Cells Reveals the Complexity and Dynamics of Mammalian Proteomes (2011) · cites this paper as Kopp et al., 1999
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References 54 · Cited by 334
- Authors
- Kopp, E., Medzhitov, R., Carothers, J., Xiao, C., Douglas, I., Janeway, C. A., & Ghosh, S.
- Affiliations
- Howard Hughes Medical Institute (US)
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 1999-08-15
- Volume
- 13
- Issue
- 16
- Pages
- 2059-2071
- ISSN
- 0890-9369 (ISSN-L)
- PMC
- PMC316957
- OpenAlex
- W2062903004
- Cited by
- 334
- References
- 54
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 7 · 2023: 6 · 2022: 12 · 2021: 9 · 2020: 12 · 2019: 8 · 2018: 6 · 2017: 12 · 2016: 5 · 2015: 8 · 2014: 12 · 2013: 1 · 2012: 9
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institutes of Health
- National Institute of Allergy and Infectious Diseases (R01-AI4334)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Keywords
- ECSIT, Toll-like receptor signaling, IL-1 signaling, NF-κB activation, TRAF6, adaptor proteins, innate immunity, signal transduction
- MeSH terms
- Amino Acid Sequence, Animals, Cell Line, Transformed, Cloning, Molecular, Drosophila, Enzyme Activation, Biological Evolution, Humans, Membrane Glycoproteins, Molecular Sequence Data, Protein Processing, Post-Translational, Proteins, Receptors, Cell Surface, Receptors, Immunologic, Saccharomyces cerevisiae, Signal Transduction, NF-kappa B, Protein Serine-Threonine Kinases, Receptors, Interleukin-1, Insect Proteins, Drosophila Proteins, TNF Receptor-Associated Factor 6, MAP Kinase Kinase Kinase 1, Adaptor Proteins, Signal Transducing, Toll-Like Receptors, Mice
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