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
- Breast cancer remains a critical worldwide health issue, accounting for approximately 2.3 million new diagnoses and 665,684 deaths in 2022, underscoring the urgent need for novel interventions. This investigation examined Cymarin's potential as an anti-breast cancer compound, focusing on MAPK8 (4L7F), through integrated network pharmacology, molecular docking, dynamics simulations, MMGBSA, ADMET, and DFT evaluations. Network analysis pinpointed 95 shared targets, constructing a PPI network with 30 nodes and 219 edges, emphasizing hub genes such as STAT3, JUN, BCL2L1, MAPK8, and MAPK1. GO enrichment highlighted signaling regulation and kinase activities, while KEGG pathways implicated oncogenic cascades, AGE-RAGE signaling, TRP-mediated inflammation, apoptosis, and insulin resistance. Docking revealed Cymarin's favorable binding affinity (-9.69 kcal/mol) compared to Tamoxifen (-9.31 kcal/mol), driven by hydrogen bonds, van der Waals, and hydrophobic contacts. A 200 ns molecular dynamics simulation suggested that the Cymarin-MAPK8 complex maintained a generally more stable dynamic profile than Tamoxifen-MAPK8. MMGBSA confirmed superior binding free energy for Cymarin (-34.58 kcal/mol) compared to Tamoxifen (-25.87 kcal/mol), primarily from van der Waals and electrostatic contributions. ADMET profiling indicated Cymarin's favorable absorption (73.688%), absence of CYP inhibition, and non-mutagenic profile. DFT metrics suggested Cymarin's enhanced stability with a slightly wider energy gap (10.5787 eV) and higher hardness (5.2894 eV). These findings position Cymarin as a compelling multi-target candidate, warranting empirical confirmation. - Source: PubMed
Publication date: 2026/04/21
Nguyen Hung Duc - Tributyl citrate (TBC), a widely used substitute for phthalate plasticizers, has shown increasing environmental accumulation, raising concerns about its potential human health risks. However, its toxicological effects, particularly regarding gastrointestinal disease progression, remain largely unexplored. In this study, animal experiments first demonstrated that TBC aggravates colonic inflammation in a mouse model of microplastic-induced colitis. Computational toxicology analysis further predicted TBC to possess potential carcinogenic properties, suggesting its role in promoting colitis-associated carcinogenesis. Using integrated bioinformatics approaches, we combined network toxicology, molecular docking, and molecular dynamics simulations to identify the putative toxicological targets and molecular pathways involved in TBC-induced inflammation-to-cancer transition. A total of 299 TBC-related targets were identified from multilevel databases, and 13 core targets were highlighted through STRING and Cytoscape analyses, including AKT2, MAPK1, MAPK3, HSP90AA1, PIK3CD, BCL2, PIK3R1, PIK3CB, ESR1, CASP3, KRAS, and ERBB2. GO and KEGG enrichment analyses indicated that TBC may drive carcinogenic progression via pathways associated with oxidative stress and inflammatory responses. Molecular docking and dynamics simulations validated the stable interactions between TBC and key targets. To further confirm TBC's role in colitis-associated tumorigenesis, we employed an AOM/DSS-induced colorectal cancer mouse model and found that TBC significantly exacerbated both intestinal inflammation and tumor formation. Transcriptomic analysis further validated the enrichment of ROS-mediated chemical carcinogenesis pathways and revealed that intestinal barrier disruption may also be a critical contributor to TBC-mediated cancer progression. Collectively, this study provides a theoretical basis for understanding the molecular mechanisms by which TBC aggravates inflammation-associated colorectal cancer, and offers a framework for risk assessment and regulatory strategies addressing plasticizer exposure in digestive health. - Source: PubMed
Publication date: 2025/10/08
Chen HaosongCheng YixianZhou YaoFu RuiJia JianguangZhang ShuyuanChen JunjieCao HaikunZhang PengGeng QilongGu JinghuaChen BoHan WenxiuXiong MaomingLi TingCao Guodong - Although the molecular mechanism by which wortmannin exerts its anticancer properties in solid tumors is not fully understood, particularly in the context of oral cancer where research is scarce, this study seeks to explore how wortmannin disrupts the PI3K pathway, consequently affecting the proliferation and apoptosis of human oral cancer cells. - Source: PubMed
Kumbhar GauriSuryawanshi PoonamLadke Vaibhav - This study integrated network pharmacology and experimental validation to elucidate the mechanism of Longdan Xiegan Pills (LDXG) in treating chronic stress-induced hypertension. Active components of LDXG were retrieved from the TCMSP database and screened based on oral bioavailability (OB) and drug-likeness (DL). Potential targets were predicted using SwissTargetPrediction. Disease targets related to hypertension were collected from OMIM and GeneCards. A compound-target network was constructed using Cytoscape, and protein-protein interaction (PPI) analysis was performed via the STRING database. Functional enrichment analysis (GO and KEGG) was conducted using DAVID. Molecular docking was performed with LeDock. In vivo, systolic and diastolic blood pressures were measured non-invasively, myocardial histopathology was evaluated by HE staining, the content of target protein in pvn and adrenal gland was measured by western blot, and serum inflammatory markers were quantified via ELISA. A total of 178 active components of LDXG were screened, Gentiana scabra Bunge (Gentian), Gardenia jasminoides Ellis (Gardeniae fructus), Scutellaria baicalensis Georgi (Huangcen), Bupleurum chinense DC (Bupleurum), and Glycyrrhiza uralensis Fisch (Licorice) were identified as the core components.The core targets included SRC, MAPK3, MAPK1, PIK3R1, RELA and STAT3. GO functional enrichment and KEGG pathway enrichment analyses indicated that LDXG primarily modulated protein kinase activity, ATP binding, protein serine/threonine kinase activity and protein kinase binding.These processes involved the PI3K-Akt, HIF-1, VEGF, ErbB and FoXO. Animal experiments demonstrated LDXG can significantly lowered blood pressure level in chronic stress-induced hypertension rats,reduced the contents of src and STAT3 in the PVN and MAPK1 in the adrenal gland and reduced serum levels of angiotensin II (Ang II), cortisol and adrenocorticotropic hormone(ACTH). LDXG can attenuate chronic stress hypertension by regulating JAK/STAT, Src/MAPK and other signaling pathways and reducing the expression of Ang II through a variety of active compounds. - Source: PubMed
Publication date: 2026/04/17
Jia HuizhuoLv MingyaoYang YingWang ZheZhang YanzhaoZhou JinxuXia LongfeiZhang JingWan HaifuLi Na - Coxsackievirus infection can cause various diseases such as myocarditis and encephalitis, posing a serious threat to human health. However, there are currently no specific therapeutic drugs or effective vaccines for Coxsackievirus infection, so exploring new anti-Coxsackievirus agents is of great significance. Geniposide, an iridoid glycoside component from traditional Chinese medicine Gardenia jasminoides, has shown multiple pharmacological activities, but its antiviral effect against Coxsackievirus and related mechanisms remain unclear. - Source: PubMed
Publication date: 2026/04/02
Xia JianboShi ZuliangShen Mengxin