ArticleThe Journal of clinical investigation2013
JUNB/AP-1 controls IFN-γ during inflammatory liver disease.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 76 citations in OpenAlex.
- Cellular antibody affinity-based CRISPR screening identifies JUNB as a broadly acting antiviral factor.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Identification and Validation of a Two-Gene NK Cell-Related Risk Model for COPD: Integration of Single-Cell and Bulk RNA-Seq Analysis.International journal of chronic obstructive pulmonary disease · 2026Article
- Liver cancer development driven by the AP-1/c-Jun~Fra-2 dimer through c-Myc.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Depletion of JunB increases adipocyte thermogenic capacity and ameliorates diet-induced insulin resistance.Nature metabolism · 2024Article
- Circadian control of ConA-induced acute liver injury and inflammatory response via Bmal1 regulation of Junb.JHEP reports : innovation in hepatology · 2023Article
- Colonic stem cell from severe ulcerative colitis maintains environment-independent immune activation by altering chromatin accessibility and global mLife medicine · 2023Article
- ScRNA-seq revealed an immunosuppression state and tumor microenvironment heterogeneity related to lymph node metastasis in prostate cancer.Experimental hematology & oncology · 2023Article
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- JunB: a paradigm for Jun family in immune response and cancer.Frontiers in cellular and infection microbiology · 2023Review
- MORA and EnsembleTFpredictor: An ensemble approach to reveal functional transcription factor regulatory networks.PloS one · 2023Article
- Microbiological Characteristics and Pathogenesis ofVeterinary sciences · 2022Article
- Regulation of Inflammation-Related Genes throughInternational journal of molecular sciences · 2022Article
- Targeting Chemotherapy to Decondensed H3K27me3-Marked Chromatin of AML Cells Enhances Leukemia Suppression.Cancer research · 2022Article
- Anlotinib Benefits theOxidative medicine and cellular longevity · 2022Article
- FosL1 Is a Novel Target of Levetiracetam for Suppressing the Microglial Inflammatory Reaction.International journal of molecular sciences · 2021Article
- The Hallmarks of Flavonoids in Cancer.Molecules (Basel, Switzerland) · 2021Review
- CD56bright cells respond to stimulation until very advanced age revealing increased expression of cellular protective proteins SIRT1, HSP70 and SOD2.Immunity & ageing : I & A · 2018Article
- The histone demethylase UTX regulates the lineage-specific epigenetic program of invariant natural killer T cells.Nature immunology · 2017Article
- Baicalein reduces angiogenesis in the inflammatory microenvironment via inhibiting the expression of AP-1.Oncotarget · 2017Article
- The Fos-Related Antigen 1-JUNB/Activator Protein 1 Transcription Complex, a Downstream Target of Signal Transducer and Activator of Transcription 3, Induces T Helper 17 Differentiation and Promotes Experimental Autoimmune Arthritis.Frontiers in immunology · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Understanding the molecular pathogenesis of inflammatory liver disease is essential to design efficient therapeutic approaches. In hepatocytes, the dimeric transcription factor c-JUN/AP-1 is a major mediator of cell survival during hepatitis, although functions for other JUN proteins in liver disease are less defined. Here, we found that JUNB was specifically expressed in human and murine immune cells during acute liver injury. We analyzed the molecular function of JUNB in experimental models of hepatitis, including administration of concanavalin A (ConA) or α-galactosyl-ceramide, which induce liver inflammation and injury. Mice specifically lacking JUNB in hepatocytes displayed a mild increase in ConA-induced liver damage. However, targeted deletion of Junb in immune cells and hepatocytes protected against hepatitis in experimental models that involved NK/NKT cells. The absence of JUNB in immune cells decreased IFN-γ expression and secretion from NK and NKT cells, leading to reduced STAT1 pathway activation. Systemic IFN-γ treatment or adenovirus-based IRF1 delivery to Junb-deficient mice restored hepatotoxicity, and we demonstrate that Ifng is a direct transcriptional target of JUNB. These findings demonstrate that JUNB/AP-1 promotes cell death during acute hepatitis by regulating IFN-γ production in NK and NKT cells and thus functionally antagonizes the hepatoprotective function of c-JUN/AP-1 in hepatocytes.
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