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
- 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 - Accumulating evidence indicates that indirubin exerts inhibitory effects on prostate cancer (PCa) progression. However, the role and underlying mechanisms of indirubin in sensitizing PCa to docetaxel remain unclear. CCK-8 assays were initially used to determine the effect of indirubin on enhancing docetaxel sensitivity in PCa cells. Following this, the expression levels of circ-Vav3 were quantified using quantitative real-time PCR (RT-qPCR) to evaluate its potential role in docetaxel resistance. Functional experiments, including flow cytometry-based apoptosis analysis and Transwell migration/invasion assays, were conducted to assess the impact of circ-Vav3 modulation and indirubin treatment on cell viability and behavior in response to docetaxel. Rescue experiments were subsequently performed to further confirm the regulatory effect of indirubin on circ-Vav3. Additionally, xenograft tumor models in nude mice were utilized to evaluate the therapeutic efficacy of indirubin in vivo. Mechanistic interactions between circ-Vav3, miR-204-5p, and MAPK1 were further investigated using RNA pulldown assays, luciferase reporter assays, and Western blot analyses. Indirubin enhanced the sensitivity of PCa cells to docetaxel by downregulating the expression of circ-Vav3, which was found to be significantly upregulated in docetaxel-resistant PCa cells. Silencing circ-Vav3 effectively reversed this resistance, as evidenced by increased apoptosis, reduced cell migration and invasion, and decreased autophagic activity. Notably, indirubin treatment suppressed circ-Vav3 expression and thereby restored docetaxel sensitivity both in vitro and in xenograft tumor models. Mechanistically, circ-Vav3 acted as a competing endogenous RNA (ceRNA) by sponging miR-204-5p, which led to the upregulation of the autophagy-related kinase MAPK1. Inhibition of MAPK1 effectively suppressed autophagy and re-sensitized docetaxel-resistant PCa cells, further confirming the critical regulatory role of the circ-Vav3/miR-204-5p/MAPK1 signaling axis in mediating chemoresistance. Our findings demonstrate that circ-Vav3 promotes docetaxel resistance in PCa by sponging miR-204-5p and subsequently activating MAPK1-mediated autophagy. Indirubin effectively restores chemosensitivity by targeting this regulatory pathway, offering a promising therapeutic strategy for overcoming chemoresistance in castration-resistant prostate cancer (CRPC). - Source: PubMed
Zheng MinghaoCai GanMa LongWu XianWang QianJin ZhenhuaZhu ChenNiu ShuaiyuPeng YanpeiXu YanTang JingyuanWei Yunfei - Polycystic ovary syndrome (PCOS) is a complex endocrine-metabolic disorder characterized by interconnected dysregulation of steroidogenesis and insulin signaling. Multi-target therapeutic strategies are increasingly needed to address its heterogeneous pathophysiology. An integrative approach combining transcriptomic analysis of GSE137684, including stratification of normoandrogenic and hyperandrogenic PCOS subtypes to capture androgen-related heterogeneity, network pharmacology, molecular docking, and in vitro validation was employed. Principal component analysis (PCA), differential expression analysis, and enrichment analyses were used to identify candidate genes and pathways. Molecular docking evaluated interactions between phytochemicals from and and key PCOS targets. Functional validation was performed in insulin-resistant 3T3-L1 adipocytes and DHEA-induced KGN cells, assessing cell viability, lipid accumulation, glucose uptake, gene expression, and hormone levels. PCA revealed partial separation between PCOS and the control samples, with PC1 and PC2 explaining 44.8% and 12.5% of variance, respectively. No genes remained significant after multiple testing correction; however, nominally significant candidates ( < 0.01) highlighted pathways related to steroidogenesis and metabolic regulation. Network analysis identified key hub genes including CYP17A1, CYP19A1, AKT1, ESR1, and MAPK1. Molecular docking demonstrated strong binding affinities, with top compounds showing binding energies up to -11.4 kcal/mol (CYP17A1) and -10.9 kcal/mol (AKT1). In vitro, cell viability remained above 80% across all tested concentrations, indicating low cytotoxicity. Treatment significantly reduced lipid accumulation and enhanced glucose uptake in insulin-resistant 3T3-L1 cells ( < 0.05). Additionally, expression of AKT1 and MAPK1 was significantly restored ( < 0.05). In KGN cells, testosterone levels were significantly decreased while the estradiol levels increased ( < 0.05), accompanied by the downregulation of CYP17A1 and upregulation of CYP19A1 ( < 0.05). The combination treatment exhibited more consistent effects across metabolic and hormonal endpoints. and exert multi-target effects on metabolic and steroidogenic pathways relevant to PCOS. This integrative study demonstrates that transcriptomics-guided network pharmacology combined with experimental validation can identify synergistic phytotherapeutic strategies for complex endocrine disorders. - Source: PubMed
Publication date: 2026/04/21
Ikrar TarunaSiahaan Salmon CharlesHendarto HendyMustika ArifaKurniawati Eighty MardiyanJatipradresthya WiskaraHadinata EdwinTaslim Nurpudji AstutiHarbuwono Dante SaksonoTjandrawinata Raymond RubiantoNurkolis Fahrul - : 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 - An integrated approach combining metabolomics, network pharmacology, and molecular docking was employed to systematically explore the serum-absorbed components of jujube, their potential targets, and regulatory pathways. UPLC-MS/MS was used to characterize the absorbed components, while network pharmacology was applied to predict potential targets associated with alcoholic liver disease (ALD). A total of 10 absorbed components and 323 common targets were identified. Among the key components, quercetin, (-)-epigallocatechin, and methyl gallate exhibited strong binding affinities to eight core targets, including AKT serine/threonine kinase 1 (AKT1) and mitogen-activated protein kinase 1 (MAPK1), with quercetin showing the highest content. Jujube intervention significantly altered the serum metabolic profiles of healthy rats, with distinct differences observed between the control and jujube-treated groups. Bioinformatics analysis revealed that the differential metabolites were mainly enriched in the diterpenoid biosynthesis pathway. These findings provide a systematic and preliminary characterization of the serum-absorbed components of jujube, their potential ALD-related targets, and their regulatory effects on serum metabolism in healthy rats. This study provides a preliminary theoretical reference and direction for further research on the potential role of jujube in ALD. - Source: PubMed
Publication date: 2026/04/17
Liu MengyuanDang YaliSuo ShikunWang YanliPan DaodongGao Xinchang