Ask about this productRelated genes to: MAPK3 antibody
- Gene:
- MAPK3 NIH gene
- Name:
- mitogen-activated protein kinase 3
- Previous symbol:
- PRKM3
- Synonyms:
- ERK1, p44mapk, p44erk1
- Chromosome:
- 16p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-05
- Date modifiied:
- 2015-09-03
Related products to: MAPK3 antibody
Related articles to: MAPK3 antibody
- Fungal infections, in particular those caused by (), pose a severe threat to human health, and the situation has been getting worse because of increasing resistance against the frontline triazole antifungals. Sea buckthorn ( L.) seed oil (SBT oil) exhibits potent antifungal activity against , principally by disrupting mitochondrial function. Its general mode of action is, nevertheless, unclear. - Source: PubMed
Publication date: 2026/04/21
Xin YanhuaQin AiyuYang JieShen YixinLi JingGuo LanyingLiang BinSu Jing - Traditional phthalate esters （PAEs） and their novel alternatives are widely used as plasticizers. Owing to their non-covalent bonding with polymer matrices， these compounds readily migrate from materials and accumulate in indoor dust， posing potential risks to human health. Although their carcinogenic and reproductive toxicities have been extensively studied， their neurotoxicity， particularly that of novel alternatives， remains poorly understood. To address this knowledge gap， this study adopted an integrated approach combining pollution profiling， health risk assessment， and mechanistic investigation to systematically evaluate the neurotoxicity risks and potential mechanisms of PAEs and their alternatives in typical campus microenvironments （classrooms， laboratories， offices， cafeterias， and dormitories）. The contamination profile of target compounds in indoor dust was determined using comprehensive two-dimensional gas chromatography coupled with time-of-flight mass spectrometry （GC×GC-TOF MS）. By integrating three exposure pathways （ingestion， inhalation， and dermal contact of dust） with absorption， distribution， metabolism， excretion， and toxicity （ADMET） models， the estimated daily intakes （EDIs） and neurotoxic health risks for different populations were assessed. Furthermore， network toxicology and molecular docking techniques were employed to elucidate the potential toxic mechanisms. Results indicated that dormitories exhibited the highest contents of target compounds， with major components including di-2-ethylhexyl phthalate （DEHP）， di（2-ethylhexyl） tetrahydrophthalate （DEHTH）， acetyl tri-n-butyl citrate （ATBC）， and trioctyl trimellitate （TOTM）. Exposure assessment identified ingestion as the predominant exposure route. Using the ADMET model， toxicity equivalency factor （TEF） and toxic equivalent quantity （TEQ） were quantified for five neurotoxicity-related health endpoints， including phenotypic neurotoxicity， estrogen receptor activity， oxidative stress， mitochondrial dysfunction， and DNA damage. Risk assessment based on TEQ revealed that females aged 18-60 years faced higher neurotoxicity risks than males， although no statistically significant gender differences in EDI were observed across all age groups. Mechanistically， network toxicology identified 59 core targets associated with neurotoxicity， including oncogene， non-receptor tyrosine kinase （SRC）， serine/threonine kinase 1 （AKT1）， estrogen receptor 1 （ESR1）， mitogen-activated protein kinase （MAPK1， MAPK3）， heat shock protein 90 alpha family class a member 1 （HSP90AA1）， and Kirsten rat sarcoma viral oncogene homolog （KRAS）. Functional enrichment analysis showed that these core targets were predominantly enriched in pathways related to endocrine resistance and cancer， suggesting that these compounds may induce neurotoxicity by disrupting cellular homeostasis and signal transduction. Molecular docking supported specific binding interactions between representative compounds and core proteins， validating the predicted associations. Notably， diphenyl phthalate （DPhP） and dicyclohexyl phthalate （DCHP） were identified as the key risk drivers. In contrast， novel alternatives with fewer aromatic rings and ester groups， such as diheptyl， -nonyl adipate （DHeNoA）， diisobutyl adipate （DiBA）， and diisodecyl adipate （DiDeA）， exhibited lower neurotoxic potential. Structure-activity relationship analysis suggested that the synergistic effect of aromatic rings and ester groups is a critical mechanism inducing neurotoxicity. By integrating environmental exposure profiling， TEQ-based risk assessment， and molecular mechanism analysis， this study not only delineates the neurotoxicity risk profile for specific campus populations but also elucidates the influence of molecular structure on neurotoxicity， providing a scientific basis for the targeted screening of low-neurotoxicity alternatives and informed risk management of indoor environmental health. - Source: PubMed
Li WeiGao KeHua KaiWang LinxiaoWei WeiLu Liping - Imidacloprid (IMI), a widely used neonicotinoid insecticide, has been associated with neurotoxic effects; however, the system-level mechanisms underlying these effects remain incompletely understood. Here, we integrated network toxicology with multi-omics analyses to investigate IMI-induced neurotoxicity in SH-SY5Y cells and the whole-organism model, Caenorhabditis elegans (C. elegans). Network toxicology identified 284 potential IMI-related targets, and protein-protein interaction network analysis further prioritized 45 core targets, including HSP90AA1, ESR1, MAPK3, SRC, MAPK1, IL6, BCL2, PRKACA, and MAPK8. Molecular docking suggested potential binding interactions between IMI and several core targets, while qRT-PCR provided transcript-level support for a subset of hub genes. Transcriptomic profiling revealed pronounced model-specific responses. In SH-SY5Y cells, IMI primarily induced neuron-related molecular alterations, characterized by disruption of voltage-gated calcium channel activity and enrichment of multiple synaptic pathways. In contrast, C. elegans exhibited broader organism-level transcriptomic remodeling involving developmental processes, extracellular structure organization, and stress-adaptive pathways, including the MAPK and FoxO signaling pathways. Untargeted metabolomics in SH-SY5Y cells further revealed biochemical remodeling related to the neuroactive ligand-receptor interaction pathway, glutathione metabolism, oxidative phosphorylation, and ABC transporter pathways. In addition, IMI significantly increased intracellular ROS levels and disrupted glutathione redox homeostasis, as reflected by altered GSH and GSSG levels and the GSH/GSSG ratio. Integrated analysis identified neuroactive ligand-receptor interaction and glutathione metabolism as shared pathway-level features across datasets, supporting a mechanistic model in which disruption of receptor-mediated neurotransmission is accompanied by redox imbalance. Overall, this study provides a systems-level view of IMI-induced neurotoxicity and highlights both shared pathway-level features and pronounced model-specific biological responses. - Source: PubMed
Publication date: 2026/05/05
Hou XingangWang KaiHou ZhiguangWei LipingZhang ZhengZheng XiaojiaoWang YuzhenLv MengTian JiangxinWang ZhaoyangMa ChaoZhao FanrongHan Jiajun - Qinggan Jiangzhi Cha (QGJZC), a compound formulation rooted in Traditional Chinese Medicine, is traditionally employed to clear heat, soothe the liver, and reduce lipid accumulation to alleviate hepatic stagnation and indigestion, aligning with modern NAFLD therapeutic strategies targeting lipid metabolism and inflammation. - Source: PubMed
Publication date: 2026/05/02
Bai YuTian ZhiliLi YinGuo XinjianGao HuiLiu YitaoMa JunLiu Fanrong - : Patients with type 2 diabetes mellitus (T2DM) undergoing cardiac surgery represent a high-risk population characterized by substantial cardiometabolic stress and increased susceptibility to postoperative heart failure, renal dysfunction, and unplanned rehospitalization. Although sodium-glucose cotransporter 2 (SGLT2) inhibitors provide established cardiorenal protection in ambulatory populations, their perioperative impact in cardiac surgery cohorts remains insufficiently defined. : In a single-center retrospective cohort of 620 T2DM patients, inverse probability of treatment weighting and time-dependent Cox regression were applied to account for perioperative treatment interruption and delayed postoperative reinitiation when evaluating the association between chronic SGLT2 inhibitor therapy and 12-month rehospitalization risk. To provide biological context for the observed clinical associations, target-driven systems pharmacology, molecular docking against SGLT2, NHE1, AMPK, and NLRP3, and protein-protein interaction (PPI) network analysis were performed. Hub proteins were identified using Maximal Clique Centrality, followed by functional enrichment (GO/KEGG) analysis. : Chronic SGLT2 inhibitor therapy was associated with reduced first rehospitalization (HR 0.64; 95% CI 0.48-0.85; = 0.002) and a lower cumulative rehospitalization burden (IRR 0.61; 95% CI 0.46-0.82; = 0.001), primarily driven by heart failure-related and metabolic phenotypes. Molecular docking analyses identified favorable binding with SGLT2 and additional cardiometabolic and inflammatory targets, including NHE1, AMPK, NLRP3, IKKβ, IL-6Rα, and PPAR isoforms, suggesting modulation of myocardial ion homeostasis, metabolic resilience, and inflammatory signaling. PPI analysis identified eight hub proteins (AKT1, MTOR, STAT3, EGFR, PIK3CA, SRC, MAPK1, and MAPK3) significantly enriched in PI3K/AKT, MAPK/ERK, and ErbB signaling pathways. : Chronic SGLT2 inhibitor therapy was independently associated with reduced postoperative rehospitalization and cumulative event burden in T2DM patients undergoing cardiac surgery. Integrated in silico analyses offer mechanistic hypotheses consistent with the observed clinical associations. These findings suggest that structured perioperative SGLT2 inhibitor management may contribute to improved postoperative outcomes, while prospective validation in future studies would strengthen these findings. However, given the retrospective observational design, these findings should be interpreted as associative rather than causal. - Source: PubMed
Publication date: 2026/04/10
Onar Lutfi CagatayGuner ErsinYilmaz Ibrahim