ReviewOncotarget2016
IκBζ: an emerging player in cancer.
Review in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 57 citations in OpenAlex.
- Adaptor proteins regulating tumor-associated macrophage polarization during cancer progression.Oncoscience · 2026Review
- Constitutive expression of the transcriptional co-activator IκBζ promotes melanoma growth and immunotherapy resistance.Nature communications · 2025Article
- The RNA binding protein Arid5a drives IL-17-dependent autoantibody-induced glomerulonephritis.The Journal of experimental medicine · 2024Article
- The Nuclear NF-κB Regulator IκBζ: Updates on Its Molecular Functions and Pathophysiological Roles.Cells · 2024Review
- Selective regulation of a defined subset of inflammatory and immunoregulatory genes by an NF-κB p50-IκBζ pathway.Genes & development · 2024Article
- Effect and mechanism of transient receptor potential canonical channel 3 on hyperoxic lung injury in neonatal rats.Pediatric discovery · 2024Article
- Genomic Analysis of Lymphoma Risk in Bullmastiff Dogs.Veterinary sciences · 2023Article
- IκBζ is an essential mediator of immunity to oropharyngeal candidiasis.Cell host & microbe · 2023Article
- Cross-talk of inflammation and chondrocyte intracellular metabolism in osteoarthritis.Osteoarthritis and cartilage · 2023Review
- The implications of alternative pre-mRNA splicing in cell signal transduction.Experimental & molecular medicine · 2023Review
- Transcriptome Analysis of Diffuse Large B-Cell Lymphoma Cells Inducibly Expressing MyD88 L265P Mutation Identifies Upregulated CD44, LGALS3, NFKBIZ, and BATF as Downstream Targets of Oncogenic NF-κB Signaling.International journal of molecular sciences · 2023Article
- IL-17A and TNF synergistically drive expression of proinflammatory mediators in synovial fibroblasts via IκBζ-dependent induction of ELF3.Rheumatology (Oxford, England) · 2023Article
- The macrophage infectivity potentiator ofFrontiers in immunology · 2023Article
- The central inflammatory regulator IκBζ: induction, regulation and physiological functions.Frontiers in immunology · 2023Review
- Inflammation suppresses DLG2 expression decreasing inflammasome formation.Journal of cancer research and clinical oncology · 2022Article
- IκB-ζ signaling promotes chondrocyte inflammatory phenotype, senescence, and erosive joint pathology.Bone research · 2022Article
- The Antidiabetic Agent Metformin Inhibits IL-23 Production in Murine Bone-Marrow-Derived Dendritic Cells.Journal of clinical medicine · 2021Article
- RTEC-intrinsic IL-17-driven inflammatory circuit amplifies antibody-induced glomerulonephritis and is constrained by Regnase-1.JCI insight · 2021Article
- Upregulation of NFKBIZ affects bladder cancer progression via the PTEN/PI3K/Akt signaling pathway.International journal of molecular medicine · 2021Article
- Regulation of theInfection and immunity · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IκBζ, an atypical member of the nuclear IκB family of proteins, is expressed at low levels in most resting cells, but is induced upon stimulation of Toll-like/IL-1 receptors through an IRAK1/IRAK4/NFκB-dependent pathway. Like its homolog Bcl3, IκBζ can regulate the transcription of a set of inflamatory genes through its association with the p50 or p52 subunits of NF-κB. Long studied as a key component of the immune response, IκBζ emerges as an important regulator of inflammation, cell proliferation and survival. As a result, growing evidence support the role of this transcription factor in the pathogenesis number of human hematological and solid malignancies.
Indexed as
Identifiers
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.