ArticlePloS one2010
An NF-kappaB-dependent role for JunB in the induction of proinflammatory cytokines in LPS-activated bone marrow-derived dendritic cells.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 45 citations in OpenAlex.
- Human Intervention Study to Assess the Effects of Supplementation with Olive Leaf Extract on Peripheral Blood Mononuclear Cell Gene Expression.International journal of molecular sciences · 2016Trial
- Early growth response protein-1 mediates lipotoxicity-associated placental inflammation: role in maternal obesity.American journal of physiology. Endocrinology and metabolism · 2013Trial
- Knockdown of JunB alleviates LPS-induced H9C2 cardiomyocyte injury and sepsis-induced myocardial injury by activating the PI3K/Akt/mTOR signaling pathway.BMC cardiovascular disorders · 2025Article
- C-terminal binding protein 2 interacts with JUNB to control macrophage inflammation.Life science alliance · 2025Article
- Circadian control of ConA-induced acute liver injury and inflammatory response via Bmal1 regulation of Junb.JHEP reports : innovation in hepatology · 2023Article
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- JunB: a paradigm for Jun family in immune response and cancer.Frontiers in cellular and infection microbiology · 2023Review
- New roles for AP-1/JUNB in cell cycle control and tumorigenic cell invasion via regulation of cyclin E1 and TGF-β2.Genome biology · 2022Article
- Modulation of Host-Parasite Interactions with Small Molecules TargetingACS infectious diseases · 2022Article
- IκBα is required for full transcriptional induction of some NFκB-regulated genes in response to TNF in MCF-7 cells.NPJ systems biology and applications · 2021Article
- Epigenetic Regulation of Vascular Smooth Muscle Cells by Histone H3 Lysine 9 Dimethylation Attenuates Target Gene-Induction by Inflammatory Signaling.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- Safflower Yellow B Protects Brain against Cerebral Ischemia Reperfusion Injury through AMPK/NF-kB Pathway.Evidence-based complementary and alternative medicine : eCAM · 2019Article
- Inferring active regulatory networks from gene expression data using a combination of prior knowledge and enrichment analysis.BMC bioinformatics · 2016Article
- Article
- JUNB is a key transcriptional modulator of macrophage activation.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
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- SUMOylation of the inducible (c-Fos:c-Jun)/AP-1 transcription complex occurs on target promoters to limit transcriptional activation.Oncogene · 2014Article
- Transcriptional complexity and roles of Fra-1/AP-1 at the uPA/Plau locus in aggressive breast cancer.Nucleic acids research · 2014Article
- Inflammatory responses in primary muscle cell cultures in Atlantic salmon (Salmo salar).BMC genomics · 2013Article
- Chromatin loop organization of the junb locus in mouse dendritic cells.Nucleic acids research · 2013Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDendritic cells (DCs) play a key role in the induction of adaptive and memory immune responses. Upon encounter with pathogens, they undergo a complex maturation process and migrate toward lymphoid organs where they stimulate immune effector cells. This process is associated with dramatic transcriptome changes, pointing to a paramount role for transcription factors in DC activation and function. The regulation and the role of these transcription factors are however ill-defined and require characterization. Among those, AP-1 is a family of dimeric transcription complexes with an acknowledged role in the control of immunity. However, it has not been studied in detail in DCs yet. METHODOLOGY/PRINCIPAL
findingsHere, we have investigated the regulation and function of one of its essential components, JunB, in primary bone marrow-derived DCs induced to maturate upon stimulation by Escherichia coli lipopolysaccharide (LPS). Our data show fast and transient NF-kappaB-dependent transcriptional induction of the junb gene correlating with the induction of the TNFalpha, IL-6, and IL-12 proinflammatory cytokines. Inhibition of JunB protein induction by RNA interference hampered the transcriptional activation of the TNF-alpha, IL-6, and IL-12p40 genes. Consistently, chromatin immunoprecipitation experiments showed LPS-inducible binding of JunB at AP-1-responsive sites found in promoter regions of these genes. Concomitant LPS-inducible NF-kappaB/p65 binding to these promoters was also observed. CONCLUSIONS/SIGNIFICANCE: We identified a novel role for JunB--that is, induction of proinflammatory cytokines in LPS-activated primary DCs with NF-kappaB acting not only as an inducer of JunB, but also as its transcriptional partner.
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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.