Human Polyclonal JunB Ab
- Known as:
- Human Polyclonal JunB Antibody
- Catalog number:
- a0774
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal JunB
Related genes to: Human Polyclonal JunB Ab
- Gene:
- JUNB NIH gene
- Name:
- JunB proto-oncogene, AP-1 transcription factor subunit
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19p13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-10
- Date modifiied:
- 2016-05-03
Related products to: Human Polyclonal JunB Ab
Related articles to: Human Polyclonal JunB Ab
- Dengue virus infection remains a major global health threat, with severe dengue disease progressing to life-threatening hemorrhage and shock syndrome. While clinical manifestations are well-documented, the transcriptional landscape associated with dengue disease severity remains incompletely understood. A multi-cohort transcriptomic analysis of public datasets was performed to establish a consensus gene expression signature of dengue virus infection. Functional enrichment and protein-protein interaction networks were used to identify biological processes and highly connected nodes. In silico drug-gene interaction analysis was conducted to prioritize candidate compounds. Clinical validation was performed using an independent cohort to assess gene expression patterns across dengue disease severity groups. Differential expression analysis revealed downregulation of interferon-related genes, including STAT1-associated pathways, alongside upregulation of stress-response genes such as CDKN1A (p21), FOS, and JUNB. Network analysis identified these genes as highly connected nodes, suggesting coordinated interplay between antiviral signaling and endothelial stress responses. Candidate compounds, including Garcinol, Paclitaxel, and Romidepsin, were identified based on curated drug-gene interactions as potential modulators of this transcriptional signature. This study defines a consensus transcriptional signature associated with dengue virus infection and dengue disease severity, highlighting coordinated changes in highly connected genes involved in host response pathways. These findings provide a framework for future experimental validation and the development of host-directed therapeutic strategies. - Source: PubMed
Publication date: 2026/06/08
Pestana Cezar RangelRodrigues Gerson Jhonatan - Metastasis is a major driver of treatment failure and mortality for gastric cancer, and the detailed cellular and molecular patterns driving tumor cells from the primary tumor to metastatic lesions remain poorly characterized. - Source: PubMed
Publication date: 2026/05/17
Sun MinWang YuanzhiZhang YuqingWang Xiaojuan - Rising temperatures driven by global warming and industrial thermal pollution are threatening the survival of both wild and farmed fish, which has emerged as one of the central concerns in international aquaculture. Understanding the physiological and behavioral responses of fish to heat exposure is critical for enhancing their survival. However, most studies rely on bulk-omic analyses at the tissue level which fail to reveal cellular heterogeneity. In the present study, ultrastructural observation and single-nuclei RNA sequencing (snRNA-seq) were applied to systematically study the physiological changes and the mechanisms of the Hucho bleekeri under acute heat stress. Histological analysis showed focal hemorrhage and lamellae broken in gill after heat stress. Ultrastructural observation revealed that after heat exposure, gill epithelial cells shed and the morphology of cell organelle damaged in pavement and mitochondria-rich cells. SnRNA-seq of gill generated 28 clusters, with the number of cells in each cluster ranging from 129 to 5590. After heat stress, epithelial (GobC) and endothelial cell proportion decreased significantly while neutrophil increased. Specifically, the change of cell proportion and pseudotime analysis indicated the occurrence of endothelial-to-mesenchymal transition during heat stress, and the expression of inflammation-related genes increased along the pseudotime axis. Differentially expressed genes (DEGs) analysis revealed that genes in heat shock protein and haemoglobin families were up-regulated in most cell type, whereas each cell also displayed specific DEGs profiles. Transcription factors analysis revealed increased activity of CEBPD, JUNB and CEBPA in most of the cell type after heat stress. Cell communication analysis showed interactions of CXCL12A-CXCR4B as well as CLDN11A-CLDN11A after heat stress. In addition, the results of snRNA-seq were validated through real-time PCR and fluorescence in situ hybridization analysis. Our study provides insights into cellular heterogeneity and physiological changes of H. bleekeri in response to heat stress, and lay a foundation for future studies on the mechanism of environmental stress on salmonid fish. - Source: PubMed
Publication date: 2026/06/06
Chen YeyuWei QinyaoWu XiaoyunYang HuanchaoLiu ZhaoChen YanlingYu YiTu QuanyuLiu GuiliangLi Hua - : Circulating tumor cells (CTCs) drive metastasis and exhibit resistance to conventional therapies, making them crucial therapeutic targets. Artesunate (AS), a derivative of artemisinin, displays anticancer activity, including inhibition of JunB proto-oncogene (JUNB) and programmed death ligand-1 (PD-L1) and upregulation of Vimentin (VIM), markers related to poor prognosis in CTCs. This study aimed to evaluate the effects of AS on adherent and non-adherent cancer cell lines (breast, lung, colon), the patient-derived colon cancer CTC-MCC-41 line, and CTCs from small-cell lung cancer (SCLC) patients. : AS's effect was evaluated using TetherChip technology. Cell viability was measured using MTT assay, while immunofluorescence staining and the VyCAP platform were applied to characterize and quantify CTCs. : AS significantly reduces viability in all tested cell lines in a time- and concentration-dependent manner, with non-adherent cells showing higher resistance. Notably, CTC-MCC-41 cells are the most sensitive to AS treatment. AS demonstrates stronger cytotoxicity than 5-fluorouracil (5-FU) in most cancer models. In SCLC patient samples, AS reduces total CTC counts ( < 0.001), eliminates aggressive phenotypes such as (CK+/CXCR4+/JUNB-) and (CK+/VIM+/GLU+), and increases apoptotic (M30+) CTCs ( = 0.021). AS additionally impairs structural features like microtentacles, which facilitate CTC reattachment. : These findings underscore AS's ability to target metastasis-competent and anoikis-resistant tumor cells, reducing their viability, invasiveness, and survival mechanisms. AS emerges as a promising candidate for anti-metastatic therapy and warrants further investigation in precision oncology. - Source: PubMed
Publication date: 2026/05/21
Pantazaka EvangeliaPapakonstantinou DimitriosRoumeliotou ArgyroGraikioti DafniTsakas SotiriosZacharopoulou NefeliMartin Stuart SKotsakis AthanasiosAthanassopoulos Constantinos MAlix-Panabières CatherineKallergi Galatea - Ischemic stroke triggers a strong neuroinflammatory response, with microglia playing dual roles in both exacerbating tissue damage and promoting repair. The molecular mechanisms regulating microglial activation and polarization remain inadequately defined. In this study, we demonstrate that the transcription factor CEBPB is a key upstream regulator of the AP-1 (JunB-Fos) complex, driving pro-inflammatory transcriptional programs in microglia following transient focal cerebral ischemia (tFCI). Transcriptomic profiling of microglia from tFCI mice revealed significant gene expression changes, particularly enrichment in inflammatory, immune, and cytokine production pathways, and identified Cebpb, Junb, Fos, and Tnf as key hub genes. Mechanistically, CEBPB is upregulated in post-ischemic microglia and directly binds to the Fos promoter to activate AP-1, inducing downstream inflammatory mediators, including IL-1β and TNF-α. Inhibition of AP-1 with the selective inhibitor T-5224 shifted microglia from a pro-inflammatory to an anti-inflammatory phenotype in vitro, decreasing pro-inflammatory cytokine production and enhancing anti-inflammatory mediator release. In vivo, T-5224 treatment in tFCI mice suppressed neuroinflammation, reduced neuronal apoptosis in the striatum and cortex, promoted a restorative microglial phenotype, and improved long-term sensorimotor and cognitive function. These findings establish the CEBPB/AP-1 axis as a critical driver of neuroinflammation in ischemic stroke and highlight it as a promising therapeutic target. - Source: PubMed
Publication date: 2026/05/26
Liang KunLu ShuangshuangShi WeihaoFan WeijianHuang YijunChen JianweiZhu Lei