ArticleNature communications2024
Molecular mechanism of IKK catalytic dimer docking to NF-κB substrates.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
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- Umbelliferone protects testes and spermatogenesis against lead acetate by effectively mitigating oxidative stress, inflammation, and apoptosis.Clinical and experimental reproductive medicine · 2026Article
- Protein-protein interaction-mediated signaling networks in ischemic stroke: from molecular mechanisms to therapeutic strategies.Acta pharmacologica Sinica · 2026Review
- Hydrogen Sulfide-Regulated NF-κB Signaling via Persulfidation: A Review.Biomolecules · 2026Review
- ASAP3 activates the NF-κB signaling pathway to promote the progression of esophageal squamous cell carcinoma.Discover oncology · 2026Article
- Hsa-miR-5585-3p regulates the NLRP3 activation and the expression of cytokines through CHUK in a cellular model of diabetic kidney disease.BMC endocrine disorders · 2026Article
- Molecular mechanisms of SIRT1 in regulating ageing and related intervention strategies.Molecular biology reports · 2026Review
- Engineering polyphenol-based osteogenic system for bone and cartilage repair: Transplantation, tissue engineering, and organoid.Journal of advanced research · 2026Review
- NEMO/IKKγ: Emerging player in the NF-κB pathway and potential therapeutic target in inflammation.Inflammation · 2026Review
- 3-carbamoyl proxyl nitroxide attenuates CClScientific reports · 2026Article
- A preliminary study on the regulatory role of phosphoribosyl pyrophosphate synthetase 2 in vesicular stomatitis virus infection.Virus genes · 2026Article
- RACK1 in host immune response to infections: molecular mechanisms and therapeutic potentials.Frontiers in immunology · 2026Review
- Natural Products Modulate Plaque Macrophage Functional Programs in Atherosclerosis.Drug design, development and therapy · 2026Review
- Design, Synthesis, Bioactivity, and Docking Studies of Isatin-Hydrazone Derivatives as Potential CDK-2 Inhibitors.Anti-cancer agents in medicinal chemistry · 2026Article
- FBXL8 Stabilizes IκBα and Negatively Regulated NF-κB Activation to Suppress Pancreatic Cancer Progression.International journal of biological sciences · 2026Article
- Protective effect of wild polysaccharides extracted fromFrontiers in pharmacology · 2026Article
- piR-37524 Overexpression in Colorectal Cancer: A Potential Diagnostic Bio-Marker and Therapeutic Target.Oncology research · 2026Article
- NSD2 mediates NF-κB and matrix metalloproteinases to drive hepatocellular carcinoma malignant progression.Translational cancer research · 2025Article
- Activation of NF-κB Signaling by Optogenetic Clustering of IKKα and β.Advanced biology · 2025Article
Corrections and comments
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Authors and funding
21 authors.
Funding
Abstract
The inhibitor of κB (IκB) kinase (IKK) is a central regulator of NF-κB signaling. All IKK complexes contain hetero- or homodimers of the catalytic IKKβ and/or IKKα subunits. Here, we identify a YDDΦxΦ motif, which is conserved in substrates of canonical (IκBα, IκBβ) and alternative (p100) NF-κB pathways, and which mediates docking to catalytic IKK dimers. We demonstrate a quantitative correlation between docking affinity and IKK activity related to IκBα phosphorylation/degradation. Furthermore, we show that phosphorylation of the motif's conserved tyrosine, an event previously reported to promote IκBα accumulation and inhibition of NF-κB gene expression, suppresses the docking interaction. Results from integrated structural analyzes indicate that the motif binds to a groove at the IKK dimer interface. Consistently, suppression of IKK dimerization also abolishes IκBα substrate binding. Finally, we show that an optimized bivalent motif peptide inhibits NF-κB signaling. This work unveils a function for IKKα/β dimerization in substrate motif recognition.
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Registered trials
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 Socratic graph.