ArticleThe Journal of biological chemistry2011
Recruitment of RelB to the Csf2 promoter enhances RelA-mediated transcription of granulocyte-macrophage colony-stimulating factor.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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.
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.
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Who cites it
11 citing papers in PubMed, 11 citations in OpenAlex.
- RelB/ILF2-GM-CSF loop sustains tumor-MDSC communication in prostate cancer immunosuppression.Cell death & disease · 2026Article
- A bioinformatics and experimental approach identifies glycoprotein-based diagnostic and prognostic biomarkers for colon adenocarcinoma.Scientific reports · 2026Article
- Targeting tumor-intrinsic S100 calcium-binding protein A1 augments antitumor immunity and potentiates immunotherapy efficacy.Signal transduction and targeted therapy · 2025Article
- Inherited human RelB deficiency impairs innate and adaptive immunity to infection.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- A T cell-intrinsic function for NF-κB RelB in experimental autoimmune encephalomyelitis.Scientific reports · 2021Article
- p(⁷⁰S⁶K¹) in the TORC1 pathway is essential for the differentiation of Th17 Cells, but not Th1, Th2, or Treg cells in mice.European journal of immunology · 2016Article
- A breast cancer stem cell niche supported by juxtacrine signalling from monocytes and macrophages.Nature cell biology · 2014Article
- Control of RelB during dendritic cell activation integrates canonical and noncanonical NF-κB pathways.Nature immunology · 2012Article
- Cooperation between classical and alternative NF-κB pathways regulates proinflammatory responses in epithelial cells.American journal of respiratory cell and molecular biology · 2012Article
- The noncanonical NF-κB pathway.Immunological reviews · 2012Review
- NIK signaling in dendritic cells but not in T cells is required for the development of effector T cells and cell-mediated immune responses.The Journal of experimental medicine · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Tumor necrosis factor (TNF) induces expression of granulocyte-macrophage colony-stimulating factor (GM-CSF) but lymphotoxin β (LTβ) does not. Here we report that priming of cells with agonistic LTβ receptor antibody synergistically enhanced TNF-induced GM-CSF expression. The LTβ priming process was not due to an increase in TNF-mediated nuclear translocation of p65, p65 DNA binding, or NF-κB transactivational activity. The synergistic effect of LTβ priming was not observed with other TNF-responsive genes such as Ccl2 or RelB, which suggested that this effect was not a general increase in TNF signaling. Furthermore, RelB and p65 were both independently recruited to the GM-CSF promoter when cells were primed with LTβ followed by TNF treatment. As a consequence, an increase in both chromatin accessibility and the recruitment of RNA polymerase II were observed to the GM-CSF promoter. Taken together, these findings suggested that LTβ signaling amplified TNF-mediated GM-CSF expression by facilitating chromatin access and the co-recruitment of RNA polymerase II to increase gene transcription. Moreover, the novel priming process described here underscores the complexity of the interactions between the classical and alternative NF-κB signaling pathways.
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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.