JNK1 (Dominant Negative) Recombinant Adenovirus
- Known as:
- JNK1 (Dominant Negative) Recombinant Adenovirus
- Catalog number:
- ADV-115
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- Cell Biolabs
- Gene target:
- JNK1 (Dominant Negative) Recombinant Adenovirus
Related genes to: JNK1 (Dominant Negative) 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 (Dominant Negative) Recombinant Adenovirus
Related articles to: JNK1 (Dominant Negative) Recombinant Adenovirus
- Cadmium (Cd) is a widespread environmental contaminant that has a detrimental impact on male reproductive toxicity (MRT) due to oxidative stress, endocrine imbalance, inflammation and cell death processes. Despite the known potential of melatonin (MLT) to ameliorate the adverse effects of Cd on MRT, the exact molecular mechanisms of such multistep action are still obscure. In this work, an integrated computational approach based on network pharmacology, protein-protein interaction (PPI) network analysis, molecular docking, MM-GBSA binding energy calculation, molecular dynamics (MD) simulation, and functional annotation was used for understanding of the molecular basis of MLT-mediated protection. Forty shared targets were found between MLT-related genes and MRT-related genes caused by cadmium exposure. Ten hub genes (PTGS2, ESR1, MAPK8, EGFR, AR, NR3C1, PGR, CCND1, MMP9, and NFKB1) were selected based on network topology analysis. Functional annotation revealed that these targets are mostly involved in steroid hormone signaling, reproductive system development, transcription regulation, inflammatory signaling, and cancer pathways. Molecular docking identified that MAPK8 and PGR are the two best-binding proteins of MLT with docking scores of -7.783 and -6.830kcal/mol, respectively and MM-GBSA binding energies of -66.10 and -63.63kcal/mol, respectively. Further MD simulations over 300ns proved to be successful in achieving a stable ligand-protein complex, maintaining structural stability, and stable binding during the course of the simulations. Taken together, these results indicate that MLT might operate via modulation of the oxidative stress-related, endocrine-related, and inflammation-related pathways simultaneously instead of operating through one specific target. - Source: PubMed
Publication date: 2026/09/10
Wanjari Uddesh RameshMukherjee Anirban GoutamJayaraman ManikandanPrabhu DhamodharanJeyaraman JeyakanthanMataghare Bhairav Chandroday - This study comprehensively employed network toxicology and experimental validation to systematically investigate the potential mechanisms by which triclosan (TCS) exacerbates rheumatoid arthritis (RA). Through multi-database screening, 173 common targets between TCS and RA were obtained. Combined with protein-protein interaction (PPI) network analysis and five machine learning algorithms, eight core hub genes (AR, CDKN1A, IGF1R, JAK2, JUN, MAPK8, MYC, and PARP1) were identified. Enrichment analysis indicated that TCS primarily interferes with signalling pathways, such as JAK-STAT, cellular senescence, and mitophagy. In vitro experiments demonstrated that TCS induces macrophage senescence and polarisation toward the M1 phenotype, promotes the expression of inflammatory cytokines, and inhibits mitophagy, leading to the accumulation of mitochondrial reactive oxygen species (ROS), loss of mitochondrial membrane potential, and impaired mitochondrial function, thereby exacerbating the inflammatory response. This study reveals that TCS may disrupt immune-metabolic homeostasis through multi-target, multi-pathway mechanisms to promote the onset and progression of RA, providing a new theoretical basis for understanding its environmental toxicity and for the prevention and treatment of RA. - Source: PubMed
Publication date: 2026/09/10
Zhang JingChen TongMa YingJieWang WenguangChen BocenJian ShaoqinXiao Man - The escalating prevalence of obesity has made it a critical public health concern. There is an urgent need to identify naturally derived compounds with anti-obesity potential. Britanin (BRI), a bioactive sesquiterpene lactone derived from Inula species, has shown promise in metabolic disorder management, but its anti-obesity mechanisms remain uncharacterized. - Source: PubMed
Zhang YiQingWu ZhiKangLi XianJiang HeZiZhou XinYuShen JinShengWang XiangyuZhang GuoXingZhou Yafeng - Emamectin benzoate (EMB) is a highly effective and widely detected environmental insecticide whose potential to induce severe cardiotoxicity and localized myocardial inflammation has raised substantial biomedical concerns. Quercetin (Que), a ubiquitous plant-derived natural antioxidant, has shown promise in mitigating exogenous chemical-induced toxicities, yet its precise immunopharmacological mechanism against EMB-induced cardiotoxicity remains to be fully elucidated. This study investigated the protective effects and mechanisms of Que. against EMB-induced cardiotoxicity by integrating network toxicology, transcriptomics, and in vivo/in vitro experimental validation. Multi-omics analysis identified MAPK8, MAPK3, and CASP3 as key responsive targets conserved across species. Functional enrichment revealed that these targets are predominantly involved in the MAPK/NF-κB signaling pathway and mitochondrial organization. Molecular docking and targeted intervention experiments confirmed that Que. potentially targets and binds to JNK (encoded by MAPK8), thereby blocking the EMB-activated signaling axis. This molecular interaction effectively restored mitochondrial dynamics and prevented mitochondrial DNA leakage into the cytoplasm, ultimately alleviating myocardial PANoptosis. Collectively, our findings demonstrate that Que. serves as a natural antagonist against chemical-induced cardiotoxicity by modulating the MAPK/NF-κB axis, offering a promising therapeutic strategy for mitigating pesticide-related immunotoxicological risks. - Source: PubMed
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