ArticleMolecular and cellular biology1999
RelB modulation of IkappaBalpha stability as a mechanism of transcription suppression of interleukin-1alpha (IL-1alpha), IL-1beta, and tumor necrosis factor alpha in fibroblasts.
Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 73 citations in OpenAlex.
- RelB/ILF2-GM-CSF loop sustains tumor-MDSC communication in prostate cancer immunosuppression.Cell death & disease · 2026Article
- MK2/p38/p53 Suppress Basal IL-1β and Non-Canonical NF-κB Signaling in Macrophages.International journal of molecular sciences · 2026Article
- NF-κB RelB suppresses the inflammatory gene expression programs of dendritic cells by competing with RelA for binding to target gene promoters.Cell discovery · 2025Article
- The path less traveled: the non-canonical NF-κB pathway in systemic lupus erythematosus.Frontiers in immunology · 2025Review
- Aryl Hydrocarbon Receptor Mechanisms Affecting Chronic Kidney Disease.Frontiers in pharmacology · 2022Review
- Transcription Analysis of the Chemerin Impact on Gene Expression Profile in the Luteal Cells of Gilts.Genes · 2020Article
- Article
- Critical role of IL-1α in IL-1β-induced inflammatory responses: cooperation with NF-κBp65 in transcriptional regulation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Noncanonical NF-κB in Cancer.Biomedicines · 2018Review
- Review
- TNF-α Modulation of Intestinal Tight Junction Permeability Is Mediated by NIK/IKK-α Axis Activation of the Canonical NF-κB Pathway.The American journal of pathology · 2016Article
- Article
- Paracrine potential of fibroblasts exposed to cigarette smoke extract with vascular growth factor induction.The Laryngoscope · 2013Article
- Autophagy protects against active tuberculosis by suppressing bacterial burden and inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Differential regulation of nuclear factor-kappa B subunits on epidermal keratinocytes by ultraviolet B and tacrolimus.The Kaohsiung journal of medical sciences · 2012Article
- The RelB subunit of NFκB acts as a negative regulator of circadian gene expression.Cell cycle (Georgetown, Tex.) · 2012Article
- Malt1-dependent RelB cleavage promotes canonical NF-kappaB activation in lymphocytes and lymphoma cell lines.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Comparative expression profiling of E. coli and S. aureus inoculated primary mammary gland cells sampled from cows with different genetic predispositions for somatic cell score.Genetics, selection, evolution : GSE · 2011Article
- Facultative heterochromatin formation at the IL-1 beta promoter in LPS tolerance and sepsis.Cytokine · 2011Article
- Classical NF-kappaB activation negatively regulates noncanonical NF-kappaB-dependent CXCL12 expression.The Journal of biological chemistry · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Members of the NF-kappaB/RelB family of transcription factors play important roles in the regulation of inflammatory and immune responses. RelB, a member of this family, has been characterized as a transcription activator and is involved in the constitutive NF-kappaB activity in lymphoid tissues. However, in a previous study we observed an overexpression of chemokines in RelB-deficient fibroblasts. Here we show that RelB is an important transcription suppressor in fibroblasts which limits the expression of proinflammatory mediators and may exert its function by modulating the stability of IkappaBalpha protein. Fibroblasts from relb(-/-) mice overexpress interleukin-1alpha (IL-1alpha), IL-1beta, and tumor necrosis factor alpha in response to lipopolysaccharide (LPS) stimulation. These cells have an augmented and prolonged LPS-inducible IKK activity and an accelerated degradation which results in a diminished level of IkappaBalpha protein, despite an upregulated IkappaBalpha mRNA expression. Consequently, NF-kappaB activity was augmented and postinduction repression of NF-kappaB activity was impaired in these cells. The increased kappaB-binding activity and cytokine overexpression was suppressed by introducing RelB cDNA or a dominant negative IkappaBalpha into relb(-/-) fibroblasts. Our findings suggest a novel transcription suppression function of RelB in fibroblasts.
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.