JunB (Ab_79) Antibody
- Known as:
- JunB (Ab_79) Antibody
- Catalog number:
- E021026-1
- Product Quantity:
- 50ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- JunB (Ab_79) Antibody
Related genes to: JunB (Ab_79) Antibody
- 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: JunB (Ab_79) Antibody
Related articles to: JunB (Ab_79) Antibody
- 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 - Memory CD8 T cells (TMEM) and exhausted CD8 T cells (TEX) are essential for host defense against infection and cancer, yet their therapeutic potential is often limited by insufficient persistence and sustained functional capacity. Strategies to enhance the longevity of both populations remain scarce. Here, we demonstrate that ablation of UBE2F, a neddylation E2 enzyme, induces a resilience program in CD8 T cells that operates across both TMEM and TEX compartments, resulting in improved viral and tumor control. This resilience state is characterized by enhanced self-renewal and survival without perturbing the conventional CD8 T cell differentiation trajectories. Mechanistically, UBE2F deficiency inhibited neddylation of CUL5, leading to accumulation of JUNB and upregulation of IL-2Rβ. The increased IL-2Rβ expression hypersensitizes CD8 T cells to physiological IL-15, thereby conferring the resilience features. Together, these findings identify the UBE2F-CUL5-JUNB-IL-2Rβ axis as a conserved posttranslational mechanism regulating CD8 T cell longevity across memory and exhausted states, providing a novel strategy for enhancing antiviral and antitumor immunity. - Source: PubMed
Publication date: 2026/05/26
Ma XiaonanGuo HenanJia YutingYin NaPeng Min - E3 ubiquitin ligases recognize substrates through specific interfaces. Accurate delineation of these interfaces is essential, as mutations disrupting them impair protein ubiquitination and drive cancer progression. However, available E3-substrate interface data are sparse and systematic prediction methods remain lacking. Here, we propose MetaESI, a deep learning framework that simultaneously predicts E3-substrate interactions and leverages its interpretable architecture to infer binding interfaces de novo. With a two-stage meta-learning strategy, MetaESI generalizes across diverse E3s and achieves state-of-the-art performance in both interaction and interface prediction. We applied MetaESI at the proteome scale to generate MetaESI-Atlas, which comprises 68,056 annotated interactions across eight species. Integrating multi-omics data, we identified mutations at MetaESI-predicted interfaces that disrupt E3-substrate binding, and experimentally validated representative examples including JunB Q244E and SPOP F102C as oncogenic drivers. By combining interpretable AI with mechanistic insight, MetaESI establishes a methodological paradigm for interpretable model design and a foundational resource for precision oncology and targeted protein degradation. - Source: PubMed
Publication date: 2026/05/20
Li DiankeZhang YutingLiu YuanZhang ZihaoQu YingjieLi JiajunJiang LinyangDiao LihongZhang ZidingZhang LingqiangCui Chun-PingLi Dong