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
- Oligoasthenozoospermia (OAS) is a major cause of male infertility. 2,8-Dihydroxyquinoline (2,8-DHQ), an endogenous antioxidant metabolite, remains unexplored in OAS. This study identified 2,8-DHQ as a bioactive XHBG metabolite and elucidated its mechanisms in improving OAS. - Source: PubMed
Publication date: 2026/09/25
Fu WeiWu SiruiYan YongtingLin MeixinDuan MeiniWu WenxiaYou Xujun - Vascular calcification is a hallmark of vascular aging that is accelerated by hyperlipidemia and contributes to adverse cardiovascular outcomes. Although vascular smooth muscle cells (VSMCs) are key mediators of vascular calcification, the signaling pathways linking aging-associated stress to osteogenic remodeling remain incompletely understood. To define the role of MAPK14 (p38α) in vascular aging, we integrated bulk RNA sequencing of young and aged mouse aortas with published single-nucleus RNA sequencing data from VSMC-specific knockout (KO) mice. Bulk RNA-seq identified age-associated activation of extracellular matrix remodeling, calcification, inflammatory, and senescence-associated gene programs, accompanied by increased p38 MAPK signaling. Single-nucleus RNA-seq further demonstrated that KO attenuated proliferative, inflammatory, fibrotic, and ossification-associated gene modules in VSMCs. Consistent with these transcriptomic findings, RUNX2 expression was markedly increased in aged aortas, whereas aged KO mice exhibited reduced RUNX2 expression together with attenuated vascular calcification, fibrosis, and inflammatory cell infiltration compared with wild-type controls. Collectively, these results identify VSMC MAPK14 as an important regulator of vascular calcification during hyperlipidemic aging and demonstrate that MAPK14 deficiency is associated with reduced RUNX2 expression and attenuated fibro-inflammatory vascular remodeling. These findings support MAPK14 as a potential therapeutic target for limiting vascular calcification and associated pathological remodeling during aging. - Source: PubMed
Publication date: 2026/09/08
Ishimwe NestorTu YuchiWang ChunhuiBryant W BartZhang WeiChen YabingLong Xiaochun - Huoxue Huayu Gel Plaster (HXHYGP) is a topical traditional Chinese medicine preparation used for oxaliplatin-induced peripheral neuropathy (OIPN), but its locally exposed bioactive components remain unclear. This study developed an integrated strategy combining pharmacodynamic evaluation, UHPLC-HRMS-based tissue pharmacochemistry, untargeted metabolomics, network pharmacology, molecular docking, and qRT-PCR to identify effective components and explore potential mechanisms. In OIPN rats, HXHYGP improved mechanical and cold sensory dysfunction; reduced plantar tissue injury and inflammatory-cell infiltration; increased nerve growth factor levels; decreased TNF-α, IL-6, and IL-1β levels; and enhanced nerve conduction velocity. A total of 496 constituents were detected in skin tissue, including 20 tissue-migrant constituents attributed to HXHYGP. Untargeted metabolomics identified 53 OIPN-related differential metabolites, of which 42 were significantly reversed after treatment. Correlation analysis and network pharmacology further identified 14 effective components and 98 common targets, with EGFR, PIK3CA, MTOR, RELA, and MAPK14 as key nodes. Molecular docking supported potential component-target interactions, while qRT-PCR confirmed reduced mRNA expression of these targets after HXHYGP treatment. These findings indicate that HXHYGP may alleviate OIPN by modulating the proposed EGFR/PI3K/AKT/mTOR/NF-κB signaling network and MAPK14-associated inflammation. This strategy provides an analytical basis for identifying pharmacodynamic substances and potential quality-marker candidates in topical traditional Chinese medicine preparations. - Source: PubMed
Hua Yu-JiaoZhang YanDing Yong-JuanChen Jing-Hua - To systematically evaluate the therapeutic effects of betulinic acid (BA) in an ankylosing spondylitis (AS) mice model and characterize the molecular changes associated with immune remodeling and Th17/Treg-related transcriptional alterations. Using β-1,3-glucan-induced SKG mice and CD3/CD28-activated Jurkat cells. Mice were divided into four groups: control (Con), AS model, methotrexate (MTX), and BA treatment. Peripheral blood mononuclear cells (PBMCs) were profiled using the 10 × Genomics single-cell transcriptomic platform, followed by T-cell subset identification, pseudotime trajectory analysis, and cell communication network reconstruction. Single-cell changes in Smad2-associated gene regulatory patterns and immune states were evaluated using scTenifoldKnk-based virtual knockout analysis. Histopathology and immunohistochemistry were used to evaluate RANK/RANKL expression in spinal tissues, while flow cytometry, immunofluorescence, ELISA, qPCR, and Western blot were performed to assess immune cell proportions, mitochondrial reactive oxygen species (ROS), and inflammatory signaling pathways. BA markedly alleviated spinal deformity, enthesitis, and bone destruction in AS mice and suppressed RANK/RANKL-mediated osteoclast activation. Single-cell transcriptomic analysis revealed pronounced Th17/Treg imbalance and activation of IL6-STAT3, MAPK/Ras, and TGF-β/SMAD signaling pathways in AS, whereas BA treatment reshaped T-cell developmental trajectories by reducing Rorc-associated differentiation while enhancing Foxp3-related dynamics. BA also disrupted the Th17-macrophage inflammatory amplification loop, reduced Th1 and Th17 populations, increased Th2 and Treg proportions (P < 0.05), and decreased mitochondrial ROS accumulation and aberrant CCR9 and TGFB1 expression. Virtual knockout analysis revealed that Smad2-associated regulatory networks were substantially influenced by the immune microenvironment. BA treatment was associated to decreased expression of inflammatory mediators and changed expression of a number of signaling molecules found through single-cell transcriptome investigations, such as ERK1/2, KRAS, MAPK14, and SMAD2, according to experimental validation (P < 0.05). BA exerts anti-inflammatory and immunomodulatory effects in AS and is associated with modulation of mitochondrial oxidative stress and multiple immune-related signaling signatures, thereby reshaping T cell developmental trajectories and contributing to partial restoration of immune homeostasis. - Source: PubMed
Publication date: 2026/09/22
Shi YinliGuan ShuangZeng GuoduanWang SicunLi MuzhiYu YananWang YuedanLiu JunYang WeibinWang Zhong - Kinases are major drug targets especially in cancer therapy. However, the high degree of conservation of their active sites hinders the development of selective inhibitors, motivating a deeper understanding of kinase conformational ensembles and allosteric communication pathways. Here, we use dynamical network analysis to identify key residues involved in a dynamic allostery between the N- and C-lobes that connects the major functional units of the MAP kinase p38α. By combining NMR spectroscopy, activity assays, and in silico analysis of wildtype protein and mutants in the presence or absence of an active-site inhibitor, we experimentally validate the obtained architecture with respect to global protein motion and long-range allosteric modulation. Notably, the identified network highlights communication pathways across several functional sites, prominently involving the allosteric site, the activation loop, and even the lipid-binding domain with its embedded cryptic pocket in the C-lobe. These findings provide mechanistic insight into p38α allostery and suggest viable opportunities for the rational design of allosteric modulators of MAP kinases. - Source: PubMed
Publication date: 2026/08/22
Roy Acharyya SuchandraWeisner JörnBernardi Rafael CLinser Rasmus