IRAK (Pelle) family member IRAK-2 and MyD88 as proximal mediators of IL-1 signaling.
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Summary
Two additional proximal mediators were identified that are required for IL-1R-induced NF-kappaB activation: IRAK-2, a Pelle family member, and MyD88, a death domain-containing adapter molecule, both associate with the IL- 1R signaling complex.
- Type
- article
- Published
- 1997-11-28
- Cited by
- 1,292
- References
- 25
- OpenAlex
- https://openalex.org/W1965971815
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:30938943
Keywords
Signal transduction, Cell biology, Kinase, Receptor, Biology
References
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- Yama/CPP32β, a mammalian homolog of CED-3, is a CrmA-inhibitable protease that cleaves the death substrate poly(ADP-ribose) polymerase
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- RAIDD is a new 'death' adaptor molecule
- MAP3K-related kinase involved in NF-KB induction by TNF, CD95 and IL-1
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- Molecular Cloning and Characterization of a Second Subunit of the Interleukin 1 Receptor Complex (*)
- IRAK: A Kinase Associated with the Interleukin-1 Receptor
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- MAP kinases in the immune response.
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- SHIP, SHIP2, and PTEN activities are regulated in vivo by modulation of their protein levels: SHIP is up-regulated in macrophages and mast cells by lipopolysaccharide.
- NF-κB translocation prevents host cell death after low-dose challenge by Legionella pneumophila
- Identification and characterization of a myeloid differentiation factor 88 (MyD88) cDNA from Zhikong scallop Chlamys farreri.
- Direct extracellular interaction between the early secreted antigen ESAT-6 of Mycobacterium tuberculosis and TLR2 inhibits TLR signaling in macrophages
- Interleukin-1 Receptor Type 1 Is a Substrate for γ-Secretase-dependent Regulated Intramembrane Proteolysis*
- Mecanismos de transducciÓn del lipopolisacárido
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- Retroviral mutagenesis in a newly developed myc transgenic mouse model of human B cell and plasma cell neoplasia
- The Host Immune Response to Streptococcus pneumoniae: Bridging Innate and Adaptive Immunity
- IFN-α/β Induction by dsRNA and Toll-Like Receptors Shortens Allograft Survival Induced by Costimulation Blockade: A Dissertation
- Characterisation of viral proteins that inhibit Toll-like receptor signal transduction.
- The forward genetic dissection of afferent innate immunity.
- Rôle fonctionnel du Toll-Like Receptor 4 exprimé par les plaquettes sanguines en tant que cellules inflammatoires de l'immunité
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