Ask about this productRelated genes to: Jund antibody
- Gene:
- JUND NIH gene
- Name:
- JunD proto-oncogene, AP-1 transcription factor subunit
- Previous symbol:
- -
- Synonyms:
- AP-1
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-10
- Date modifiied:
- 2016-10-11
Related products to: Jund antibody
Related articles to: Jund antibody
- The mechanisms underlying gastric cancer (GC) progression, including recurrence and metastasis, remain unclear. Studies have reported that microRNAs and Men1 are closely associated with multiple tumors, including GC. Therefore, assessing the impact of Men1 on GC and investigating the underlying mechanisms are essential. - Source: PubMed
Publication date: 2026/05/06
Jiang Jin-XunZhang Shi-JieZhao KunZheng Kai-TianWang Shan-HuChen Tian-deWang Zhen - Alcohol use disorder (AUD) is a complex polygenic disease. Rodent models of alcohol dependence have been instrumental in modeling various aspects of dependence. Single-nucleus transcriptomics has enabled the profiling of cell-type-specific changes in gene expression in both human AUD and animal models. In this study, we identified shared dysregulated transcriptomic networks (TN), comprising gene co-expression modules and gene regulatory networks (GRNs) in a mouse model of alcohol dependence and individuals with AUD. Through cell-type-specific TN analysis, we identified translationally relevant, conserved dependence dysregulated molecular signatures. We identified conserved dependence-upregulated gene co-expression modules in astrocytes and oligodendrocytes, with hub genes Slc1a3 and Pde4b, respectively. These genes are linked to alcohol dependence mechanisms, such as glutamate signaling, a well-established target of alcohol's effects, and PDE4, whose inhibition has been shown to reduce alcohol intake in preclinical and clinical studies. We then integrated publicly available human and mouse GRN data to identify upstream regulators of alcohol-dysregulated gene signatures in each cell type. This approach revealed a set of transcription factors (TFs), including Mef2a, Mef2c, Jund, Nr3c1, and Zeb1, that were upstream of most dysregulated genes in both the mouse and human datasets and have established relevance to addiction biology, representing promising targets for translational research. Collectively, these findings demonstrate the utility of cross-species, cell-type-specific network analysis for uncovering conserved molecular mechanisms in alcohol dependence. The identification of shared dysregulated networks, cell type homology, and upstream regulators provides a foundation for developing translationally relevant targeting strategies that can be tested in animal models. - Source: PubMed
Publication date: 2026/04/21
Salem NihalWarden AnnaRoberts AmandaRoberto MarisaMayfield R Dayne - With the rapid development of cancer treatment, immunotherapy has revolutionized renal cell carcinoma (RCC) treatment, yet patient responses remain heterogeneous. Here, a computational pipeline was constructed by integrating single-cell and bulk RNA sequencing data to identify immune-related candidate driver genes and characterize their impact on RCC immunotherapy. Based on gene regulatory networks (GRN), 25 immune-related candidate driver genes were identified, leading to the stratification of patients into three clusters (C1-C3). Compared to the C2/C3 cluster, the C1 cluster exhibited elevated immune infiltration, tumor mutation burden and checkpoint expression, which may represent immunotherapy responders. Dynamic analysis of GRNs revealed the critical role of candidate driver genes in predicting the efficacy of immunotherapy. , and in lymphoid cells of C1 participated in anti-tumor immune response by impacting target genes , , and . , , , and were up-regulated in clusters C2 and C3, leading to tumor progression and immune evasion by influencing target genes , and . In conclusion, integration of the transcriptome with molecular networks provided a network-based framework to uncover immune-related candidate driver genes for stratifying RCC patients, thereby serving as potential therapeutic targets to improve the outcome of RCC immunotherapy. - Source: PubMed
Publication date: 2026/04/13
Yin XiangzheWang LuSun YanwuLi ShiyiYu WentongWang SiyaoGeng ZhichaoZhao HongyingWang Li - Liver progenitor-like cells (LPLCs) are essential for liver regeneration during some injury process, yet their epigenetic characters remain poorly understood. Using single-nucleus assay for transposase-accessible chromatin sequencing (snATAC-seq), we profiled chromatin accessibility in a mouse model of 3,5-diethoxycarbonyl-1,4-dihydrocollidin (DDC) diet-induced cholestasis at six time points: homeostasis (D0), injury (D8, D17), and repair (R2, R7, R21). We analyzed 75,452 high-quality nuclei, identifying 15 liver cell types, including LPLCs. Among 221,845 accessible chromatin regions, 192,079 showed differential accessibility. LPLCs exhibited enriched binding motifs for SWI/SNF (SMARCC1) and AP-1 (FOS, JUND and JUNB) complexes, highlighting their roles in transcriptional regulation. This study provides a comprehensive chromatin accessibility landscape of liver injury and regeneration, suggesting SWI/SNF and AP-1 as potential therapeutic targets. - Source: PubMed
Publication date: 2026/05/02
Wu HongYang YongqingWu YanXu JiangshanGuo PengchengLiu ShipingHou YongHao Shijie - Fibrotic diseases, driven by excessive extracellular matrix deposition, account for substantial global morbidity and mortality, yet effective therapies remain elusive. Emerging evidence highlights impaired protein homeostasis as a key contributor to fibrosis, prompting exploration of autophagy-mediated degradation pathways. Here, we investigate the role of chaperone-mediated autophagy (CMA), a selective lysosomal degradation mechanism, in fibrosis progression. We demonstrate that CMA activity is suppressed in fibrotic tissues from experimental mice and human patients, correlating with pathological SMAD2/4 accumulation. Mechanistically, CMA deficiency impedes SMAD2/4 degradation, amplifying TGF-β signaling and collagen overproduction. AAV-mediated LAMP2A overexpression to restore CMA activity alleviated bleomycin-induced pulmonary fibrosis and carbon tetrachloride-induced hepatic fibrosis in mice. Furthermore, we identify sunitinib, an FDA-approved tyrosine kinase inhibitor, as a novel CMA activator that enhances LAMP2A transcription via targeting the transcription factor JUND, reduces SMAD2/4 levels, and mitigates fibrosis in vivo. Our findings establish CMA dysfunction as a common pathological hallmark of fibrotic diseases and unveil therapeutic strategies targeting CMA to restore protein homeostasis. This study provides critical insights into fibrosis pathogenesis and positions pharmacological CMA activation as a promising treatment avenue. CMA is impaired across fibrotic tissues, driving disease progression. Sunitinib activates CMA by targeting JUND to promote SMAD2/4 degradation, suppressing TGFβ-SMADs-fibrosis signaling. CMA, chaperone-mediated autophagy; IPF, idiopathic pulmonary fibrosis; PF, pulmonary fibrosis; HF, hepatic fibrosis. - Source: PubMed
Publication date: 2026/04/30
Jin Jia-YuanSong Yu-XuanLu Jia-BinLi Guan-QunWang Jun-QiangFeng Xue-JingLuo Pei-HuaYang BoXu Zhi-FeiYan HaoHe Qiao-JunYang Xiao-Chun