ArticleMolecular and cellular biology2001
Interleukin-1 (IL-1) receptor-associated kinase leads to activation of TAK1 by inducing TAB2 translocation in the IL-1 signaling pathway.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed, 198 citations in OpenAlex.
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- Mitochondrial P-JNK target, SAB (SH3BP5), in regulation of cell death.Frontiers in cell and developmental biology · 2024Review
- Smyd3 negatively regulates the anti-viral pathway by promoting TAK1 degradation in teleost fish.Journal of virology · 2023Article
- Effects of TmTak1 silencing on AMP production as an Imd pathway component in Tenebrio molitor.Scientific reports · 2023Article
- microRNA-149-5p mediates the PMCell biology and toxicology · 2023Article
- Activity-Based Protein Profiling Reveals Potential Dasatinib Targets in Gastric Cancer.International journal of molecular sciences · 2020Article
- Synthesis and biological activity of 2-cyanoacrylamide derivatives tethered to imidazopyridine as TAK1 inhibitors.Journal of enzyme inhibition and medicinal chemistry · 2020Article
- New Selective Progesterone Receptor Modulators and Their Impact on the RANK/RANKL Complex Activity.Molecules (Basel, Switzerland) · 2020Article
- Article
- Pharmacological inhibition of TAK1, with the selective inhibitor takinib, alleviates clinical manifestation of arthritis in CIA mice.Arthritis research & therapy · 2019Article
- TAK1/Map3k7 enhances differentiation of cardiogenic endoderm from mouse embryonic stem cells.Journal of molecular and cellular cardiology · 2019Article
- TAK1 mediates convergence of cellular signals for death and survival.Apoptosis : an international journal on programmed cell death · 2019Review
- EnterohemorrhagicEmerging microbes & infections · 2019Article
- The Regulation of JNK Signaling Pathways in Cell Death through the Interplay with Mitochondrial SAB and Upstream Post-Translational Effects.International journal of molecular sciences · 2018Review
- An Update on Autoinflammatory Diseases: Relopathies.Current rheumatology reports · 2018Review
- Sophocarpine attenuates wear particle-induced implant loosening by inhibiting osteoclastogenesis and bone resorption via suppression of the NF-κB signalling pathway in a rat model.British journal of pharmacology · 2018Article
11 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-1 (IL-1) is a proinflammatory cytokine that recognizes a surface receptor complex and generates multiple cellular responses. IL-1 stimulation activates the mitogen-activated protein kinase kinase kinase TAK1, which in turn mediates activation of c-Jun N-terminal kinase and NF-kappaB. TAB2 has previously been shown to interact with both TAK1 and TRAF6 and promote their association, thereby triggering subsequent IL-1 signaling events. The serine/threonine kinase IL-1 receptor-associated kinase (IRAK) also plays a role in IL-1 signaling, being recruited to the IL-1 receptor complex early in the signal cascade. In this report, we investigate the role of IRAK in the activation of TAK1. Genetic analysis reveals that IRAK is required for IL-1-induced activation of TAK1. We show that IL-1 stimulation induces the rapid but transient association of IRAK, TRAF6, TAB2, and TAK1. TAB2 is recruited to this complex following translocation from the membrane to the cytosol upon IL-1 stimulation. In IRAK-deficient cells, TAB2 translocation and its association with TRAF6 are abolished. These results suggest that IRAK regulates the redistribution of TAB2 upon IL-1 stimulation and facilitates the formation of a TRAF6-TAB2-TAK1 complex. Formation of this complex is an essential step in the activation of TAK1 in the IL-1 signaling pathway.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.