Ask about this productRelated genes to: MAPK1 antibody
- Gene:
- MAPK1 NIH gene
- Name:
- mitogen-activated protein kinase 1
- Previous symbol:
- PRKM2, PRKM1
- Synonyms:
- ERK, ERK2, p41mapk, MAPK2
- Chromosome:
- 22q11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-05
- Date modifiied:
- 2019-04-23
Related products to: MAPK1 antibody
Related articles to: MAPK1 antibody
- Liver fibrosis is a progressive pathological process triggered by chronic liver disorders, which may progress to hepatocellular carcinoma (HCC) if left untreated. Currently, there are no specific therapeutic agents for liver fibrosis, highlighting an urgent need for novel pharmacological strategies. Tomatidine (TD), a major steroidal glycoal-kaloid abundant in immature tomato fruits, leaves, and stems, exhibits diverse biological activities including anti-inflammation, anti-tumor effects, and autophagy regulation. However, its role in liver fibrosis and the underlying molecular mechanisms remain incompletely understood. In this study, we combined network pharmacology, molecular docking, and experimental validation to investigate the potential effects of TD against liver fibrosis and its associated mechanism of action. In vitro experiments using the human hepatic stellate cell (HSC) line LX-2 demonstrated that TD inhibited HSC proliferation in a dose- and time-dependent manner, and downregulated the expression of fibrosis-related markers α-smooth muscle actin (α-SMA) and collagen type I α1 chain (COL1A1) at the gene, protein, and cellular levels. Network pharmacology analysis identified 18 common targets between TD and liver fibrosis, with core targets including MAPK3, RELA, and MAPK1 involved in intracellular signal transduction and stress-activated MAPK cascade. Although no autophagy-related targets were identified in the current database among these common targets, pharmacological evidence and experimental validation confirmed that TD promoted autophagy in LX-2 cells, as indicated by reduced P62 expression, increased LC3-II/LC3-I ratio and Beclin-1 levels, and enhanced autophagic flux. Further mechanism exploration revealed that TD exerted its autophagy-promoting effect by regulating the ERK/MAPK-mTOR-ULK1 signaling pathway: TD suppressed the phosphorylation of ERK and mTOR, while activating ULK1 phosphorylation. Molecular docking verified stable binding affinity between TD and key proteins in this pathway (ERK, MAPK, mTOR, ULK1) as well as autophagy-related proteins (P62, Beclin-1, LC3) and fibrosis-related protein COL1A1, with specific amino acid residues mediating hydrogen bond formation. Collectively, our findings demonstrate that TD modulates fibrosis-related markers in hepatic stellate cells by promoting autophagy in HSCs via the ERK/MAPK-mTOR-ULK1 pathway. This study enriches the biological function research of TD and provides a novel potential candidate and theoretical basis for the development of anti-liver fibrosis therapeutics. - Source: PubMed
Publication date: 2026/05/08
Fan YutingZhang YuxinLi WeitongDu YinSong YangWang JinhuiTang BinDeng FengmeiCheng Li - N-acyl amino acids (N-acyl AAs) are potential bioactive compounds in fermented soybean (FS), but their accurate annotation is challenging due to their structural diversity, the existence of various isomers and wide polarity differences. Herein, we established a novel One-pot Micro Synthesis-Chemical Derivatization (OMSCD)-LC-MS analytical approach for comprehensive profiling of N-acyl AAs. First, the rapid synthesis of 142 N-acyl AA standards combined with in situ DIAAA derivatization in a one-pot manner significantly enhanced ionization and separation efficiency, particularly enabling excellent discrimination of isomers. Next, using this method, 222 N-acyl AAs were rapidly identified in FS, of which 200 were reported for the first time. Among them, N-oleoyl AAs, present at high contents in FS, demonstrated significant anti-liver cancer activity in a cell model, with MAPK1 acting as a promising candidate target. Overall, the OMSCD-LC-MS strategy facilitates the N-acyl AAs profiling, offering new preliminary insights into the functional components of FS. - Source: PubMed
Publication date: 2026/05/05
Han JieLi YujieAo LanjiaZhang LiZhou TingtingLi NaWu Jian-Lin - 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 - Gastrointestinal symptoms in Parkinson's disease (PD), in particular chronic constipation, are common and are treated in China using the traditional Chinese medicine (Jia-Wei-Ji-Chuan-Jian decoction) (JWJCJ)). However, information on therapeutic targets and the underlying mechanism is limited. - Source: PubMed
Publication date: 2026/05/05
Loong Shi KayWu FeifeiLiu YizhouVoratunyakit NapattharinWei ShangyuLi WeiLi RuiPan Weidong