ArticleThe Journal of biological chemistry2008
Stabilization of RelB requires multidomain interactions with p100/p52.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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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.
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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.
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Who cites it
48 citing papers in PubMed, 62 citations in OpenAlex.
- Potentiation of noncanonical NF-κB signaling and marginal zone B cell expansion by CARD11-mediated regulation of p100 processing.Cell reports · 2025Article
- 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
- NF-κB: master regulator of cellular responses in health and disease.Immunity & inflammation · 2025Review
- Nuclear Factor-Kappa B Regulation of Osteoclastogenesis and Osteoblastogenesis.Endocrinology and metabolism (Seoul, Korea) · 2023Article
- NFκB pathway dysregulation due to reduced RelB expression leads to severe autoimmune disorders and declining immunity.Journal of autoimmunity · 2023Article
- The NF-κB multidimer system model: A knowledge base to explore diverse biological contexts.Science signaling · 2023Review
- Aspergillus fumigatus Drives Tissue Damage via Iterative Assaults upon Mucosal Integrity and Immune Homeostasis.Infection and immunity · 2023Article
- Atypical IκB Bcl3 enhances the generation of the NF-κB p52 homodimer.Frontiers in cell and developmental biology · 2022Article
- RelB and Neuroinflammation.Cells · 2021Review
- Targeting NF-κB with Nanotherapy in a Mouse Model of Adult T-Cell Leukemia/Lymphoma.Nanomaterials (Basel, Switzerland) · 2021Article
- Nfkb2 variants reveal a p100-degradation threshold that defines autoimmune susceptibility.The Journal of experimental medicine · 2021Article
- Origin of the Functional Distinctiveness of NF-κB/p52.Frontiers in cell and developmental biology · 2021Review
- Expression of p52, a non-canonical NF-kappaB transcription factor, is associated with poor ovarian cancer prognosis.Biomarker research · 2020Article
- Biological characteristics of transcription factor RelB in different immune cell types: implications for the treatment of multiple sclerosis.Molecular brain · 2019Review
- Germinal center B cell initiation, GC maturation, and the coevolution of its stromal cell niches.Immunological reviews · 2019Review
- Aberrant splicing of the tumor suppressor CYLD promotes the development of chronic lymphocytic leukemia via sustained NF-κB signaling.Leukemia · 2018Article
- Retinol dehydrogenase-10 promotes development and progression of human glioma via the TWEAK-NF-κB axis.Oncotarget · 2017Article
- Article
- Tumor-suppressor NFκB2 p100 interacts with ERK2 and stabilizes PTEN mRNA via inhibition of miR-494.Oncogene · 2016Article
- Non-canonical NF-κB pathway activation predicts outcome in borderline oestrogen receptor positive breast carcinoma.British journal of cancer · 2016Article
Corrections and comments
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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
The NF-kappaB family member RelB has many properties not shared by other family members such as restricted subunit association and lack of regulation by the classical IkappaB proteins. We show that the protein level of RelB is significantly reduced in the absence of p100 and reduced even more when both p100 and p105 are absent. RelB stabilizes itself by directly interacting with p100, p105, and their processed products. However, RelB forms complexes with its partners using different interaction modes. Although the C-terminal ankyrin repeat domain of p105 is not involved in the RelB-p105 complex formation, all domains and flexible regions of each protein are engaged in the RelB-p100 complex. In several respects the RelB-p52 and RelB-p100 complexes are unique in the NF-kappaB family. The N-terminal domain of p100/p52 interacts with RelB but not RelA. The transcriptional activation domain of RelB, but not RelA, directly interacts with the processing region of p100. These unique protein-protein contacts explain why RelB prefers p52 as its dimeric partner for transcriptional activity and is retained in the cytoplasm as an inhibited complex by p100. This association-mediated stabilization of RelB implies a possible role for RelB in the processing of p100 into p52.
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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 OpenQuestion graph.