MAPK14 (phospho-Tyr182) Antibody
- Known as:
- MAPK14 (phosphorilated-Tyr182) Antibody
- Catalog number:
- abx000291
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- MAPK14 (phospho-Tyr182) Antibody
Related genes to: MAPK14 (phospho-Tyr182) Antibody
- Gene:
- MAPK14 NIH gene
- Name:
- mitogen-activated protein kinase 14
- Previous symbol:
- CSPB1, CSBP1, CSBP2
- Synonyms:
- PRKM14, p38, Mxi2, PRKM15
- Chromosome:
- 6p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1995-01-24
- Date modifiied:
- 2016-10-05
Related products to: MAPK14 (phospho-Tyr182) Antibody
Related articles to: MAPK14 (phospho-Tyr182) Antibody
- Sepsis and postoperative delirium (POD) may share inflammatory and neuroimmune mechanisms, but their common molecular basis remains unclear. This study aimed to identify candidate shared molecular targets and explore a clinically feasible pharmacological candidate linked to the prioritized target. - Source: PubMed
Publication date: 2026/08/26
Kong Wei-JiaXue Jing-XianYu LeiZhou Qing-ShanZhang Huai-QiJin JunDeng Jiang-Tao - This study aimed to identify pulmonary hypertension (PH)-associated molecular biomarkers and candidate small-molecule compounds using public transcriptomic data and independent validation resources. Three Gene Expression Omnibus datasets (GSE22356, GSE33463, and GSE48149) were integrated following normalization, probe annotation, and ComBat batch-effect correction. Differential expression analysis, weighted gene co-expression network analysis, functional enrichment analysis, protein-protein interaction network analysis, and three machine-learning algorithms were used to identify core feature genes. Diagnostic performance was evaluated using receiver operating characteristic curves. External validation included an independent lung-tissue cohort (GSE117261), a pulmonary artery single-cell RNA-sequencing dataset (GSE210248), and quantitative reverse transcription PCR validation in independent lung-tissue samples. Connectivity Map-based drug repositioning and molecular docking were used to screen candidate compounds. Seventy-eight differentially expressed genes were identified, and CXCL10, JUN, IFIH1, MX1, and TLR7 were selected as core feature genes. In the independent GSE117261 lung-tissue cohort, JUN showed the strongest external support, whereas replication of the other genes was variable. Quantitative reverse transcription PCR in 20 biologically independent pulmonary arterial hypertension samples and 20 control samples confirmed upregulation of all five genes. The apparent five-gene qRT-PCR model and 100 repeated stratified five-fold cross-validation analyses both yielded an area under the curve of 1.000, although the small cohort requires cautious interpretation and independent prospective validation. Single-cell analysis of GSE210248 supported altered communication between immune and structural cells and smooth muscle cell phenotypic switching. BRD-K91900765/VX-745 ranked highest in Connectivity Map screening. MAPK14/p38α, its established pharmacological target, was included as a positive-reference docking protein, whereas docking against the five biomarker-associated proteins was treated as exploratory. These findings support the five genes as candidate PH biomarkers and VX-745 as a computational drug-repositioning hypothesis requiring experimental validation. - Source: PubMed
Publication date: 2026/08/25
Jiang ChenglangLiang JuanchuangJiang Xianghui - Perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) are well-known neurodevelopmental toxicants, but the potential molecular mechanism needs to be further clarified. This study aimed to investigate the underlying mechanism of PFOA and PFOS-induced neurodevelopmental toxicity by integrating network toxicology, transcriptomic data from autism spectrum disorder patients and study. Network toxicology identified 42 core targets that enriched in a total of 105 significant GO entries and 142 KEGG pathways. With the disease-context comparison from the transcriptomic, 10 hub targets and 22 common KEGG pathways were identified. Cellular senescence-associated responses including cellular senescence and cell cycle were proposed as one of the potential mechanisms underlying PFOA and PFOS co-exposure-induced neurodevelopmental toxicity. Molecular docking analysis showed that PFOA and PFOS elicits potential binding capacities with hub targets, with TP53 and MAPK 13 exhibiting lower binding affinities with both PFASs, further predicting the potential role of these targets in PFASs-induced neurodevelopmental toxicity. After PFOA and PFOS co-treatment, reduced cell viability, a senescence-like phenotype characterized by cell cycle arrest and increased positive senescence β-galactosidase, upregulation of senescence-associated biomarkers including TP53, p53, p21 and IL-6 as well as the significant up-regulation of , , and genes were observed in human neuroblastoma SH-SY5Y cells. Thereafter, these findings suggested the multi-target and multi-pathway characteristic of PFOA and PFOS co-exposure-induced neurodevelopmental toxicity with cellular senescence-associated responses as one of the potential molecular mechanisms. - Source: PubMed
Publication date: 2026/08/24
Xin LiliGuo RuiSun JiaweiSu YueCai JiahangLi WanzhenWan ZhongxiaoWang Jianshu - 6PPD and its ozonation product 6PPD-quinone (6PPD-Q) are widespread tire-derived pollutants. This study combined network toxicology, clinical transcriptomics, molecular docking, and experimental validation to investigate their intestinal toxicity mechanisms and potential molecular relevance to inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC). Database screening identified 213 predicted targets for 6PPD and 165 for 6PPD-Q. Venn analysis identified 160 and 61 targets shared between 6PPD and CD- and UC-associated genes, respectively, whereas 112 and 105 targets were shared between 6PPD-Q and CD- and UC-associated genes, respectively. Network analyses showed that 6PPD-associated targets were mainly enriched in inflammatory signaling and oxidative stress-related pathways involving candidate hubs such as HIF1A, IL1B, IL6, and PTGS2. In comparison, 6PPD-Q-associated targets were enriched in kinase-signaling and mucosal-repair-related pathways involving HCK, KDR, LYN, EGFR, and MAPK14. Molecular docking predicted favorable binding poses between the compounds and the selected candidate targets, with docking scores ranging from -6.0 to -8.8 kcal/mol. Comparisons with clinical transcriptomic datasets further showed that several candidate targets were dysregulated in inflamed IBD tissues. In vivo, repeated exposure of C57BL/6 mice to 6PPD or 6PPD-Q for 40 days resulted in colon injury, reduced expression of intestinal tight-junction proteins, and increased expression of inflammatory mediators. In RAW264.7 macrophages, both compounds induced dose-dependent cytotoxicity, ROS production, and increased proinflammatory gene expression. These findings demonstrate that 6PPD and 6PPD-Q induce intestinal injury, oxidative stress, and inflammatory activation in experimental models and affect molecular targets and pathways implicated in IBD. Further studies using established experimental IBD models are warranted to determine whether these compounds exacerbate pre-existing intestinal inflammation or influence disease severity. - Source: PubMed
Publication date: 2026/08/22
Zhang YixuanLuo YuyangWang SiyiLi Ze - The pathological progression of sepsis is closely associated with T cell senescence. However, the key signaling pathways regulating this process and potential therapeutic drug remain unclear. - Source: PubMed
Publication date: 2026/08/06
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