JNK1 Recombinant Adenovirus
- Known as:
- JNK1 Recombinant Adenovirus
- Catalog number:
- ADV-114
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- Cell Biolabs
- Gene target:
- JNK1 Recombinant Adenovirus
Related genes to: JNK1 Recombinant Adenovirus
- Gene:
- MAPK8 NIH gene
- Name:
- mitogen-activated protein kinase 8
- Previous symbol:
- PRKM8
- Synonyms:
- JNK, JNK1, SAPK1
- Chromosome:
- 10q11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-28
- Date modifiied:
- 2016-10-05
Related products to: JNK1 Recombinant Adenovirus
Related articles to: JNK1 Recombinant Adenovirus
- Triphala is a traditional three-fruit formulation with potential anticancer activity, but its ferroptosis-related mechanisms in oral cancer remain unclear. We integrated network pharmacology, transcriptomic analyses, prognostic modeling, Mendelian randomization, immune and drug-response analyses, molecular docking, and in vitro validation to investigate the Triphala-ferroptosis-oral cancer axis. Fifty-eight candidate functional genes were identified, and an eight-gene signature comprising AKR1C3, CA9, EGFR, GSTA1, MAPK8, MGST1, PPARG, and RB1 showed prognostic value across multiple cohorts. Mendelian randomization supported causal associations of MAPK8, MGST1, and PPARG with oral cancer risk. Seven Triphala-derived compounds, including epigallocatechin gallate, quercetin, kaempferol, luteolin, ellagic acid, gallic acid, and quinine, displayed favorable predicted interactions with key targets. In CAL-27 cells, Triphala altered the expression of signature genes, reduced GPX4 and SLC7A11 protein levels, increased Feand malondialdehyde, depleted glutathione and glutathione peroxidase activity, and enhanced lipid peroxidation; these effects were partially modulated by ferrostatin-1. This study advances the field by linking Triphala to a ferroptosis-based prognostic framework and experimentally demonstrating its regulation of the SLC7A11-GSH-GPX4 axis in oral cancer. - Source: PubMed
Zhao YiweiLi SiminJiang LinxinKreher DeborahSchmalz GerhardFichter AndreasHu Xianda - Pancreatic cancer is a highly lethal digestive malignancy characterized by insidious onset and rapid progression. Approximately 80% of patients are diagnosed at an advanced stage with metastasis, missing the opportunity for radical surgery, and chemotherapy remains the main palliative treatment. Its incidence is rising annually, highlighting the urgent need for novel therapeutic strategies. MLN4924 (Pevonedistat), a first-in-class NEDD8-activating enzyme inhibitor, exhibits promising antitumor activity in various cancers, yet its role and mechanism in pancreatic cancer remain largely undefined. Potential hub targets of MLN4924 in pancreatic cancer were screened using Swiss Target-Prediction and Gene-Cards databases. Western blot was used to detect the expression of hub genes and the activity of the prostaglandin G/H synthase 2 (PTGS2)-epidermal growth factor receptor (EGFR)-phosphatidylinositol 3-kinase (PI3K)/RAC-gamma serine/threonine-protein kinase (Akt)/serine/threonine-protein kinase (mTOR) axis following MLN4924 intervention. CCK-8, EdU, and wound-healing assays were performed to evaluate cell proliferation and migration after MLN4924 treatment. Furthermore, PTGS2 knockdown via siRNA transfection was applied to verify its effects on EGFR-PI3K/Akt/mTOR pathway activity, malignant phenotypes, and gemcitabine sensitivity in pancreatic cancer cells. We identified four hub genes (CASP3, PTGS2, MMP9, and MAPK8) of MLN4924 in pancreatic cancer. We validated that MLN4924 suppressed proliferation and migration of pancreatic cancer cells, downregulated hub gene expression, and inhibited the PTGS2-mediated PI3K/AKT/mTOR signaling pathway. Furthermore, siRNA-mediated silencing of PTGS2 phenocopied the inhibitory effects of MLN4924 on cell proliferation. Notably, both MLN4924 and PTGS2 knockdown significantly enhanced the chemosensitivity of pancreatic cancer cells to gemcitabine. Collectively, our results demonstrate that MLN4924 exerts antitumor effects in pancreatic cancer by targeting the PTGS2-EGFR-PI3K/AKT/mTOR axis, providing a mechanistic rationale for its clinical application in pancreatic cancer therapy. - Source: PubMed
Publication date: 2026/08/11
Wang MinMou YuQiu Ji-YinHe Xiao-FengTang CanZhu Hai-Tao - Enterovirus A71 (EV-A71) is a major causative agent of hand, foot, and mouth disease, yet no specific antiviral therapy has been approved. This study systematically evaluated the efficacy and mechanisms of alkaloids against EV-A71 infection by integrating meta-analysis, network pharmacology, and molecular docking. Nine animal studies were included. Meta-analysis suggested that alkaloid intervention significantly improved survival (OR = 30.62, 95% CI: 10.44-89.82), reduced clinical severity, attenuated body weight loss, and decreased viral loads in infected tissues. Subgroup analyses preliminarily suggested that quinolizidine alkaloids and high-dose regimens (>5 mg/kg) may be associated with preclinical intervention effects. Network pharmacology predicted 155 shared targets between seven active alkaloids and EV-A71-related genes, with MAPK1, MAPK3, JUN, AURKB, and MAPK8 recognized as core targets through computational screening. Functional enrichment analysis suggested significant involvement of the MAPK, TNF, and IL-17 signaling pathways. Molecular docking provided computational support for stable binding affinities between active alkaloids and core targets (-6.7 to -9.3 kcal/mol). Collectively, these findings suggest that alkaloids exert anti-EV-A71 effects through both direct antiviral activity and host-directed regulatory mechanisms, supporting their potential as candidates for the development of novel anti-EV-A71 therapeutics. - Source: PubMed
Publication date: 2026/07/23
Xie WenzhanLv LinxiWang TianWei JialongGui YanshanGu WeiFeng Hui - Classic Hodgkin lymphoma (CHL) is a highly curable disease. However, a subset of patients develops relapsed/refractory disease, underscoring the need for predictors of treatment response. Although immune-checkpoint inhibitors have improved outcomes, many patients still experience suboptimal responses. A deeper understanding of the CHL transcriptomic landscape may improve patient stratification and guide treatment approaches. Targeted mRNA-NGS was performed on formalin-fixed paraffine-embedded CHL-tissue using the HTG EdgeSeq Precision Immune-Oncology Panel (1,392 genes) in treatment-naive and post-chemotherapy relapsed treated with nivolumab-based protocols. Differential gene expression and pathway enrichment analyses were conducted to characterize tumor-intrinsic, and microenvironmental features associated with disease biology and treatment response. Across all CHL samples (n = 25) we observed overexpression of immune-checkpoint and immunoregulatory genes (CD274, CTLA-4, IL6, IL13), and markers of macrophage-rich/matrix-remodeling microenvironment (CD163, MMP2, TIMP1), alongside loss of B-cell identity and tumor suppression programs. Pathways analysis revealed activation of IL6/JAK/STAT3, TNF-α/NF-κB, KRAS-UP, and Inflammatory response, with reduced proliferative and metabolic activity. Immunotherapy non-responders, both in the overall (n = 5; 20%), and the treatment-naïve CHL (n = 2; 12%) displayed a proliferative, cytokine-activated, and immunologically cold phenotype. This includes shared overexpression of FADD, NFKB1, and TGFB1 and downregulation of SMAD7, together with activation of E2F, G2M, MYC, and PI3K/AKT/mTOR pathways and negative enrichment of TNF-α/NF-κB, IL6/JAK/STAT3, and Inflammatory response. Post-chemotherapy relapsed (n = 8) exhibited adaptative immunoregulatory and stress response signatures (IL15, TNFSF18, MAPK8, FUT4), along with reduced immune activation and loss of tumor-suppressor signaling. This study highlights the biological complexity and transcriptional diversity underlying CHL and its tumor microenvironment. Immunotherapy non-responders exhibited an "oncogene-driven" transcriptional profile independent of previous treatment status, whereas responders showed an "inflammatory immune-scape" phenotype, offering insight into mechanisms of resistance. Despite the limited sample size, these findings provide a foundation for larger precision-focused studies aimed at improving outcomes in CHL. - Source: PubMed
Publication date: 2026/08/05
Hamana LeticiaMarques-Piubelli Mario LWei LuKhan KhajaKakarala LakshmiShen LiWistuba Ignacio ILee Hun JuSolis Luisa MVega Francisco - Mitochondrial dysfunction is a critical early driver of endothelial injury in atherogenesis. Natural plant-derived products targeting mitochondrial quality control represent a promising therapeutic approach, yet their mechanisms in oxidized LDL (ox-LDL)-induced endothelial damage remain underexplored. - Source: PubMed
Publication date: 2026/07/21
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