ReviewOncogene2006
IkappaB kinase complexes: gateways to NF-kappaB activation and transcription.
Review in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 344 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
344 citing papers in PubMed, 647 citations in OpenAlex.
- Osimertinib Resistance in EGFR-Mutated Non-Small Cell Lung Cancer: Mechanisms and Therapeutic Strategies.MedComm · 2026Review
- Integrating Divergence-Based Proteomic Analysis and Directed Network Diffusion to Characterize Diagnosis-Anchored Molecular Variability at the Metabolic Syndrome-Migraine Interface.International journal of molecular sciences · 2026Article
- Immune-Enhancement Effects of 6-Methoxykaempferol on Cyclophosphamide-Induced Immunosuppression via Improving Antioxidant Enzyme Expression, NF-κB and MAPK Signaling, and Modulating Gut Microbiome.Antioxidants (Basel, Switzerland) · 2026Article
- Clinical Significance of IKBKB Mutations:Saudi medical journal · 2026Review
- SUMOylation protects against sepsis-associated acute kidney injury by stabilizing IκBα.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Ferroptosis-neuroinflammation interplay: mechanistic pathways and therapeutic opportunities in central nervous system disorders.Frontiers in aging neuroscience · 2026Review
- WNT signalling promotes NF-κB activation and drug resistance in KRAS-mutant colorectal cancer.EMBO reports · 2025Article
- Differential effects of flunixin meglumine and meloxicam on TNF- α production in LPS-stimulated equine neutrophils in vitro.Veterinary and animal science · 2025Article
- Proliferative Effect of Proanthocyanidins on HGF-1 and HPDLF Cells: An In Vitro Study.Medicina (Kaunas, Lithuania) · 2025Article
- TNF-α in traumatic brain injury: a bidirectional effect in regulating neuroimmune and inflammatory responses.Cellular and molecular life sciences : CMLS · 2025Review
- Silencing of lncRNA Gm26917 Attenuates Alveolar Macrophage-mediated Inflammatory Response in LPS-induced Acute Lung Injury Via Inhibiting NKRF Ubiquitination.Inflammation · 2025Article
- Repurposing Saroglitazar for neurodegenerative disorders: insight into molecular signalling pathways and neuroprotective modulations.Inflammopharmacology · 2025Review
- Article
- Analogue information processing in NF-κB gene regulatory system.Royal Society open science · 2025Article
- Senescent macrophages in cancer: roles in tumor progression and treatment opportunities.Cancer biology & medicine · 2025Review
- Dual-specific autophosphorylation of kinase IKK2 enables phosphorylation of substrate IκBα through a phosphoenzyme intermediate.bioRxiv : the preprint server for biology · 2025Article
- 1'-Acetoxychavicol Acetate Selectively Downregulates Tumor Necrosis Factor Receptor-Associated Factor 2 (TRAF2) Expression.Molecules (Basel, Switzerland) · 2025Article
- Enhancing MyD88 oligomerization is one important mechanism by which IBDV VP2 induces inflammatory response.PLoS pathogens · 2025Article
- Resiquimod induces a mixed Th1 and Th2 response via STAT1 and STAT3 signalling in chickens.Biochemistry and biophysics reports · 2025Article
- BEV 2C protein inhibits the NF-κB signalling pathway to promote viral replication by targeting IKBKB and p65.Veterinary research · 2025Article
284 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcription factors of the NF-kappaB family regulate hundreds of genes in the context of multiple important physiological and pathological processes. NF-kappaB activation depends on phosphorylation-induced proteolysis of inhibitory IkappaB molecules and NF-kappaB precursors by the ubiquitin-proteasome system. Most of the diverse signaling pathways that activate NF-kappaB converge on IkappaB kinases (IKK), which are essential for signal transmission. Many important details of the composition, regulation and biological function of IKK have been revealed in the last years. This review summarizes current aspects of structure and function of the regular stoichiometric components, the regulatory transient protein interactions of IKK and the mechanisms that contribute to its activation, deactivation and homeostasis. Both phosphorylation and ubiquitinatin (destructive as well as non-destructive) are crucial post-translational events in these processes. In addition to controlling induced IkappaB degradation in the cytoplasm and processing of the NF-kappaB precursor p100, nuclear IKK components have been found to act directly at the chromatin level of induced genes and to mediate responses to DNA damage. Finally, IKK is engaged in cross talk with other pathways and confers functions independently of NF-kappaB.
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What OpenQuestion holds
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 OpenQuestion graph.