ArticleProceedings of the National Academy of Sciences of the United States of America2014
IKK phosphorylates RelB to modulate its promoter specificity and promote fibroblast migration downstream of TNF receptors.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- RelB/ILF2-GM-CSF loop sustains tumor-MDSC communication in prostate cancer immunosuppression.Cell death & disease · 2026Article
- The alternative NF-κB RelB subunit is a novel critical sensor of lipid metabolism to promote tumor development.Cell death & disease · 2026Article
- CK2 promotes jasmonic acid signaling response by phosphorylating MYC2 in Arabidopsis.Nucleic acids research · 2023Article
- Cancer resistance via the downregulation of the tumor suppressorsExploration of targeted anti-tumor therapy · 2023Review
- The Alternative RelB NF-kB Subunit Exerts a Critical Survival Function upon Metabolic Stress in Diffuse Large B-Cell Lymphoma-Derived Cells.Biomedicines · 2022Article
- RelB and Neuroinflammation.Cells · 2021Review
- miR-200a contributes to the migration of BMSCs induced by the secretions of E. faecalis via FOXJ1/NFκB/MMPs axis.Stem cell research & therapy · 2020Article
- Tumor necrosis factor receptor family costimulation increases regulatory T-cell activation and function via NF-κB.European journal of immunology · 2020Article
- Biological characteristics of transcription factor RelB in different immune cell types: implications for the treatment of multiple sclerosis.Molecular brain · 2019Review
- Article
- Immune Differentiation Regulator p100 Tunes NF-κB Responses to TNF.Frontiers in immunology · 2019Article
- Noncanonical NF-κB in Cancer.Biomedicines · 2018Review
- Non-canonical NFκB mutations reinforce pro-survival TNF response in multiple myeloma through an autoregulatory RelB:p50 NFκB pathway.Oncogene · 2017Article
- Article
- Review
- Review
- Astrocyte Transcriptome from the Mecp2(308)-Truncated Mouse Model of Rett Syndrome.Neuromolecular medicine · 2015Article
- Targeting signaling factors for degradation, an emerging mechanism for TRAF functions.Immunological reviews · 2015Review
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TNFα is a potent cytokine that plays a critical role in numerous cellular processes, particularly immune and inflammatory responses, programmed cell death, angiogenesis, and cell migration. Thus, understanding the molecular mechanisms that mediate TNFα-induced cellular responses is a crucial issue. It is generally accepted that global DNA binding activity of the NF-κB avian reticuloendotheliosis viral (v-rel) oncogene related B (RelB) subunit is not induced upon TNFα treatment in fibroblasts, despite its TNFα-induced nuclear accumulation. Here, we demonstrate that RelB plays a critical role in promoting fibroblast migration upon prolonged TNFα treatment. We identified the two kinases IκB kinase α (IKKα) and IκB kinase β (IKKβ) as RelB interacting partners whose activation by TNFα promotes RelB phosphorylation at serine 472. Once phosphorylated on serine 472, nuclear RelB dissociates from its interaction with the inhibitory protein IκBα and binds to the promoter of critical migration-associated genes, such as the matrix metallopeptidase 3 (MMP3). Further, we show that RelB serine 472 phosphorylation status controls MMP3 expression and promigration activity downstream of TNF receptors. Our findings provide new insights into the regulation of RelB activity and reveal a novel link between selective NF-κB target gene expression and cellular response in response to TNFα.
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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.