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GENE:

JUNB (JunB Proto-Oncogene AP-1 Transcription Factor Subunit)

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Other names: JUNB, JunB Proto-Oncogene AP-1 Transcription Factor Subunit, Transcription Factor Jun-B, Jun B Proto-Oncogene, Activator Protein 1, AP-1
Associations
9d
Non-enzymatic function of QSOX2 directly regulates the JUNB-ITGB4 axis and enhanced resistance to osimertinib in EGFR-mutation lung adenocarcinoma. (PubMed, Cell Death Discov)
In conclusion, this study innovatively identified the non-enzymatic function of QSOX2 in regulating OR in EGFR-mutant LUAD through the JUNB-ITGB4-FAK/AKT pathway. The QSOX2/JUNB-ITGB4 signaling axis represents a potential therapeutic target for overcoming OR and offers a novel strategy to improve outcomes in LUAD patients.
Journal
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EGFR (Epidermal growth factor receptor) • ITGB4 (Integrin Subunit Beta 4) • JUNB (JunB Proto-Oncogene AP-1 Transcription Factor Subunit)
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EGFR mutation
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Tagrisso (osimertinib)
17d
Glyphosate-Induced Metabolic and Immune Modulation in Hepatoma Cells: Identification of Key Genes as Diagnostic and Therapeutic Targets Using an In Silico Systems Biology Approach. (PubMed, J Xenobiot)
Notably, all hub genes demonstrated strong diagnostic performance, highlighting their potential as sensitive biomarkers of glyphosate exposure. Collectively, this study provides comprehensive insights into gene expression changes associated with glyphosate exposure in hepatoma cells, linking them to hepatic metabolic dysregulation and immune modulation and suggesting a panel of hub genes with potential diagnostic and therapeutic significance.
Journal
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TNFA (Tumor Necrosis Factor-Alpha) • PIK3R1 (Phosphoinositide-3-Kinase Regulatory Subunit 1) • CEBPA (CCAAT Enhancer Binding Protein Alpha) • CD36 (thrombospondin receptor) • ALDOA (Aldolase Fructose-Bisphosphate A) • ATF3 (Activating Transcription Factor 3) • JUNB (JunB Proto-Oncogene AP-1 Transcription Factor Subunit) • PFKFB3 (6-Phosphofructo-2-Kinase/Fructose-2,6-Biphosphatase 3) • PGK1 (Phosphoglycerate Kinase 1) • PNPLA3 (Patatin Like Phospholipase Domain Containing 3) • PPARA (Peroxisome Proliferator Activated Receptor Alpha)
1m
Alveolar echinococcosis drives functional reprogramming of hepatic CD8+ T cells. (PubMed, Front Cell Infect Microbiol)
AE infection drives a transition from acute inflammation to chronic immune regulation through extensive lineage diversification and functional reprogramming of CD8+ T cells. Spatially organized DC-T-cell interactions likely contribute to maintaining a regulated yet immunologically active microenvironment, providing insights for targeting chronic-stage immune responses in AE.
Journal
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CD8 (cluster of differentiation 8) • TNFAIP3 (TNF Alpha Induced Protein 3) • THY1 (Thy-1 membrane glycoprotein) • ITGAX (Integrin Subunit Alpha X) • NR4A1 (Nuclear Receptor Subfamily 4 Group A Member 1) • JUNB (JunB Proto-Oncogene AP-1 Transcription Factor Subunit) • ADGRE5 (Adhesion G Protein-Coupled Receptor E5)
1m
Integrated transcriptomics and molecular docking identify hub genes and statin regulators in Helicobacter pylori-associated gastric mucosal pathogenesis. (PubMed, Front Cell Infect Microbiol)
To explore potential therapeutic interventions, we performed small-molecule drug prediction and molecular docking for hub genes revealed: Simvastatin: Linked to CCL20, NFKBIA, and ICAM1. Atorvastatin: Associated with CDKN1A, ICAM1, and TNF. TPCA-1: Targeting JAK1. These findings provide a theoretical foundation for further investigation into the molecular mechanisms underlying H. pylori-related diseases.
Journal
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BRCA1 (Breast cancer 1, early onset) • CXCL8 (Chemokine (C-X-C motif) ligand 8) • BIRC3 (Baculoviral IAP repeat containing 3) • JAK1 (Janus Kinase 1) • TNFAIP3 (TNF Alpha Induced Protein 3) • CCL20 (C-C Motif Chemokine Ligand 20) • ICAM1 (Intercellular adhesion molecule 1) • IRF1 (Interferon Regulatory Factor 1) • ITGAM (Integrin, alpha M) • SPI1 (Spi-1 Proto-Oncogene) • ETS1 (ETS Proto-Oncogene 1) • IL17A (Interleukin 17A) • STAT1 (Signal Transducer And Activator Of Transcription 1) • CDKN1A (Cyclin-dependent kinase inhibitor 1A) • NFKB2 (Nuclear Factor Kappa B Subunit 2) • NFKBIA (NFKB Inhibitor Alpha 2) • NFKBIE (NFKB Inhibitor Epsilon) • TRAF1 (TNF Receptor Associated Factor 1) • CXCL1 (Chemokine (C-X-C motif) ligand 1) • E2F1 (E2F transcription factor 1) • EGR1 (Early Growth Response 1) • HSF1 (Heat Shock Transcription Factor 1) • JUNB (JunB Proto-Oncogene AP-1 Transcription Factor Subunit)
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simvastatin • atorvastatin
3ms
A Meta-Analysis of the Effects of Chronic Stress on the Prefrontal Transcriptome in Animal Models and Convergence With Existing Human Data. (PubMed, Brain Behav)
Our study demonstrates that chronic stress induces a robust, cross-paradigm PFC signature characterized by downregulation of glia/myelin and vascular pathways and suppression of immediate-early gene activity, highlighting cellular processes linking chronic stress exposure, PFC dysfunction, and psychiatric disorders.
Clinical • Preclinical • Retrospective data • Review • Journal
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DUSP1 (Dual Specificity Phosphatase 1) • JUNB (JunB Proto-Oncogene AP-1 Transcription Factor Subunit)
4ms
Single-Cell Transcriptomic Analysis Reveals RNA-Binding Protein Dysregulation in Immune Checkpoint Inhibitor-Induced Colitis. (PubMed, J Leukoc Biol)
These findings highlight the regulatory role of RBPs in ICI-induced colitis and identify cell-type-specific alterations that may drive disease progression. Importantly, we pinpoint immune checkpoint-related RBPs as potential therapeutic targets, offering new strategies to manage this clinically significant irAE.
Journal • Checkpoint inhibition • IO biomarker
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PTPRC (Protein Tyrosine Phosphatase Receptor Type C) • HSPA1A (Heat Shock Protein Family A (Hsp70) Member 1A) • JUNB (JunB Proto-Oncogene AP-1 Transcription Factor Subunit) • ZFP36 (ZFP36 Ring Finger Protein)
4ms
Assessment of peripheral gene expression signatures as predictive biomarkers for hepatocellular carcinoma following DAA treatment. (PubMed, J Genet Eng Biotechnol)
PBMC expression showed high diagnostic accuracy (AUROC > 0.92 for SPHK1, WNT10A, JUNB). In conclusion, combining PBMC gene expression profiling with in-silico analyses highlights JUNB, WNT10A, SPHK1, EDN1, and KLF4 as promising non-invasive biomarker panel for HCC risk in DAA-SVR patients, reflecting their integration into epigenetic and oncogenic networks and supporting their potential for risk stratification and therapeutic targeting.
Journal
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KLF4 (Kruppel-like factor 4) • JUNB (JunB Proto-Oncogene AP-1 Transcription Factor Subunit) • SPHK1 (Sphingosine Kinase 1)
4ms
Architecture of the neutrophil compartment. (PubMed, Nature)
Finally, we show that NeuMap enables inference of the pathophysiological state of the host by profiling blood neutrophils. Our study delineates the global architecture of the neutrophil compartment and establishes a framework for exploration and exploitation of neutrophil biology.
Journal
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CSF2 (Colony stimulating factor 2) • TGFB1 (Transforming Growth Factor Beta 1) • IFNB1 (Interferon Beta 1) • JUNB (JunB Proto-Oncogene AP-1 Transcription Factor Subunit)
4ms
Comprehensive analysis of gene expression alterations in breast cancer patients via PKCθ-TBK1-mTORC1 signaling pathway. (PubMed, BMC Cancer)
The relative expression of PRKCQ and its associated signaling components suggests their critical role in breast cancer progression. These molecules, especially PRKCQ, may serve as potential biomarkers for early detection and prognosis, as well as targets for therapeutic intervention following further validation.
Journal • BRCA Biomarker
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BRCA (Breast cancer early onset) • CDKN1A (Cyclin-dependent kinase inhibitor 1A) • JUNB (JunB Proto-Oncogene AP-1 Transcription Factor Subunit) • TBK1 (TANK Binding Kinase 1)
4ms
Multi-omics elucidation of KDM5C, KDM6A, and KMT2B roles in cancer epigenetic dysregulation and transcriptional reprogramming. (PubMed, Commun Biol)
Finally, integrative analyzes demonstrated strong correlations between promoter accessibility, transcription factor occupancy, and gene expression, and uncovered cooperation between epigenetic and genetic drivers. Together, these findings reveal context-dependent functional hierarchies among HMEs and underscore the necessity of multi-layered analyses to resolve the complexity of epigenetic regulation in cancer.
Journal
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KDM6A (Lysine Demethylase 6A) • KDM5C (Lysine Demethylase 5C) • GATA2 (GATA Binding Protein 2) • KMT2B (Lysine Methyltransferase 2B) • TP73 (Tumor Protein P73) • JUNB (JunB Proto-Oncogene AP-1 Transcription Factor Subunit) • PATZ1 (POZ/BTB And AT Hook Containing Zinc Finger 1) • HOXA10 (Homeobox A10)
4ms
Oncogenic KRAS/ERK/JUNB signaling suppresses differentiation regulator GATA6 in pancreatic cancer. (PubMed, J Clin Invest)
Our study identifies how oncogenic KRAS/ERK signaling suppresses GATA6 to cause dedifferentiation in pancreatic cancer. Combining KRAS/ERK inhibitors with standard-of-care chemotherapies could be a promising therapeutic strategy for treating pancreatic cancers.
Journal
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KRAS (KRAS proto-oncogene GTPase) • GATA6 (GATA Binding Protein 6) • JUNB (JunB Proto-Oncogene AP-1 Transcription Factor Subunit)
5ms
AP-1 mediated chromatin changes govern alveolar type 2 cell transition in lung injury-repair. (PubMed, bioRxiv)
Facultative stem cells balance between their resting mode and regenerative mode. In the lung, alveolar type 2 (AT2) cells produce surfactants at baseline and, upon injury, activate to self-renew and differentiate into alveolar type 1 (AT1) cells. Such activation, observed in acute lung injury, fibrosis, and tumorigenesis, proceeds through a high-KRT8 transitional phase. Using multiomic profiling and mouse genetics, we identify activator protein-1 (AP-1) transcription factors as central regulators of a CLDN4⁺ transitional substate, promoting AT2 cell dispersion, fibroblast signaling, and region-specific AT1 differentiation. AP-1 activation is conserved during oncogenic transformation in both mouse and human lungs. These findings refine our understanding of AT2 cell fate transition and chromatin dynamics, and reinforce a molecular connection between alveolar repair and tumorigenesis.
Journal
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KRAS (KRAS proto-oncogene GTPase) • JUNB (JunB Proto-Oncogene AP-1 Transcription Factor Subunit)