MAPK14 (phospho-Tyr182) Antibody
- Known as:
- MAPK14 (phosphorilated-Tyr182) Antibody
- Catalog number:
- abx000139
- 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
- UV radiation (UVR), a known skin-stressor causing inflammation, aging and carcinogenesis, activates the arylhydrocarbon receptor (AhR) and downstream molecules which are crucially involved in photo-induced skin damage. In this study, the potent UV protector melatonin was investigated regarding UVR-mediated activation of AhR and downstream molecules including tumor suppressor p27, DNA double-strand break marker pH2AX, cyclooxygenase-2 (COX-2), mitogen-activated protein kinase-14 (MAPK14)/p38α, matrix metalloproteinase-2 (MMP2) and tissue inhibitor of matrix metalloproteinase-1 (TIMP1). They were studied in ex vivo human full-thickness skin irradiated with UVA/B light (0, 300 mJ/cm) 0 h and 24 h post UV exposure, comparing skin pre-incubated with or without melatonin. Protein expression was analysed by immunofluorescence staining, gene expression by real-time qPCR. UV exposure significantly up-regulated AhR (p < 0.0001), p27 (p < 0.001) and pH2AX (p < 0.0001) protein expression 0 h and 24 h post-irradiation which was significantly counteracted by melatonin (10 M) at both time points. Further, melatonin significantly reduced gene expression of AhR by 21.2% (p < 0.01), p27 by 24.8% (p < 0.01), COX-2 by 42.9% (p < 0.001), MAPK14 by 6.6% (p < 0.05) and MMP2 by 8.2% (p < 0.05), and caused a 10.2% (n.s.) TIMP1 reduction tendency 24 h post-irradiation. Thus, melatonin prevented UV-dependent expression of AhR and downstream regulators of AhR-mediated processes possibly related to inflammation, cellular aging and carcinogenesis on protein and gene level in UV-irradiated skin. - Source: PubMed
Pustelnik KatharinaBurner TeresaHoetzenecker WolframFischer Tobias W - Developmental plasticity, or the ability of early embryonic cells to contribute to multiple lineages, is traditionally considered equal among sister blastomeres during early cleavage. However, divergence may occur earlier than expected. We performed single-cell RNA sequencing of bovine embryos from the 2- to 8-cell stages to examine transcriptional asymmetry. While gene expression was uniform at the 2-cell stage, variability increased at the 4-cell stage and became pronounced by the 8-cell stage. At this stage, blastomeres showed heterogeneity in MAPK pathway genes (e.g., RAC1, MAPK14) and the trophectoderm marker CDX2. These differences were associated with blastomere size; as larger blastomeres exhibited molecular and functional features associated with an increased propensity to generate trophectoderm cells. Thus, sister blastomeres exhibited progressive transcriptional divergence prior to compaction in bovine embryos, and these early differences may influence subsequent lineage trajectories. - Source: PubMed
Publication date: 2026/05/07
Koyama HinataMashiko DaisukeFerré-Pujol PilarSuzuki UtanoMorita ReiKaneda MasahiroKhurchabilig AtchalaltTsuji HaruhisaYao TatsumaSugimura Satoshi - The degradation of plastic waste leads to the release of numerous chemical additives, including phthalate plasticizers, which have been implicated in the pathogenesis of metabolic disorders. Di (2-ethylhexyl) phthalate (DEHP) is a widely used plasticizer whose primary metabolite, mono (2-ethyl-5-carboxypentyl) phthalate (MECPP), has been associated with multiple metabolic diseases. In this study, we applied an integrated approach combining network toxicology and molecular docking to systematically investigate the potential mechanistic role of MECPP in metabolic dysregulation. Our strategy included multi-platform target prediction, disease gene association analysis, functional enrichment, protein-protein interaction network construction, and molecular docking analysis. The results suggested that MECPP may be associated with six common core targets, including BCL2, BCL2L1, MAPK14, MMP2, MMP9, and TNFRSF1A, which are mainly involved in apoptosis, inflammatory regulation, and extracellular matrix remodeling. Pathway enrichment analysis further indicated the potential involvement of several disease-overlapping pathways, including insulin resistance, neuroactive ligand-receptor interaction, efferocytosis, advanced glycation end product-receptor for advanced glycation end product (AGE-RAGE) signaling, phospholipase D signaling, and renin secretion. Overall, these findings suggest that MECPP may contribute to metabolic dysregulation through overlapping molecular mechanisms across multiple diseases. This study provides a computational basis for future experimental validation and environmental risk assessment. - Source: PubMed
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