MAP2K3 (phospho-Ser189) Antibody
- Known as:
- MAP2K3 (phosphorilated-Ser189) Antibody
- Catalog number:
- abx000143
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- MAP2K3 (phospho-Ser189) Antibody
Related genes to: MAP2K3 (phospho-Ser189) Antibody
- Gene:
- MAP2K3 NIH gene
- Name:
- mitogen-activated protein kinase kinase 3
- Previous symbol:
- PRKMK3
- Synonyms:
- MEK3, MKK3, MAPKK3
- Chromosome:
- 17p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-11-11
- Date modifiied:
- 2016-10-05
Related products to: MAP2K3 (phospho-Ser189) Antibody
Related articles to: MAP2K3 (phospho-Ser189) Antibody
- The mechanisms underlying the predilection of atopic dermatitis for the antecubital and popliteal fossae remain unexplored. This preliminary exploratory study aimed to characterize the proteomic features of typical flexural atopic dermatitis lesions using proteomics integrated with animal model validation and to clarify the therapeutic mechanisms of Aida lotion. - Source: PubMed
Publication date: 2026/03/31
Liu FangrongLi MinGong JianYe JunhongQiu ShanyuXu KeLiu QiaoWu Weiwei - Contrast-induced acute kidney injury (CI-AKI) is a major cause of hospital-acquired AKI, but its molecular pathogenesis remains incompletely understood. In this study, we used quantitative 4D proteomics, integrating ion mass-to-charge ratio (m/z), retention time, ion intensity, and ion mobility, to profile renal tissues from a novel rat CI-AKI model based on renal venous congestion and contrast exposure, with sham-operated rats as controls. Differentially expressed proteins were identified and analyzed using pathway enrichment and protein-protein interaction (PPI) network approaches, followed by experimental validation. Using nominal screening criteria (|log2FC| ≥ 1.5 and < 0.05), we identified 180 candidate differentially expressed proteins, including 92 upregulated and 88 downregulated proteins. Pathway-level analyses showed coordinated upregulation of complement-related proteins, including C3/C5 convertase-related components and terminal pathway proteins, such as C9, together with a C4 isoform annotated as C4a in the reference database. Coagulation and fibrinolysis pathways were also markedly altered, including fibrinogen chains (FGA, FGB, FGG), PLAU, SERPINA1, and SERPINF2. In contrast, proteins associated with AMPK and MAPK signaling (including HNF4α, PRKAA2, PRKAB1, and MAP2K3) were reduced. These pathway-level changes were supported by RT-qPCR and immunohistochemical analyses. Collectively, our findings support a multidimensional injury network in rat CI-AKI involving complement activation, coagulation-fibrinolysis dysregulation, and impaired metabolic/stress-response signaling, and provide a proteomic resource for future mechanistic and translational studies. - Source: PubMed
Publication date: 2026/04/14
Yang QiangSun LimingZhang ZhijianYan ZhixinZhang JianHu JiachangDing Xiaoqiang - Rare-earth elements are extensively employed across diverse industrial sectors, increasingly raising concerns about their potential health hazards in both occupational and environmental contexts. Samarium oxide (SmO), a routinely processed rare-earth product, reproducibly precipitates pulmonary fibrosis in experimental models, yet the molecular circuitry that transduces its fibrogenic signal remains almost entirely unmapped. This study aims to elucidate the role of miR-214-3p in SmO-induced pulmonary fibrosis and to investigate its regulatory mechanism at the molecular level. A murine model of pulmonary fibrosis was established via intratracheal instillation of SmO, and histopathological changes were assessed using hematoxylin and eosin (H&E) and Masson's trichrome staining. RNA sequencing was performed on lung tissues to identify differentially expressed mRNAs. Leveraging our previously generated miRNA landscape of SmO-exposed lungs, we subjected the dataset to Gene Ontology and KEGG enrichment analyses, which convergently identified miR-214-3p as the top-ranking candidate regulator of the fibrogenic MAPK axis. The direct targeting of MAP2K3 by miR-214-3p was validated using a dual-luciferase reporter assay. Expression levels of fibrotic markers (α-SMA, Collagen I) and key components of the MAPK signaling pathway (MAP2K3, p-MAPK14, MST1) were quantified in both in vivo and in vitro models using qRT-PCR and Western blotting. Gain- and loss-of-function studies, complemented by rescue assays, were performed in human embryonic lung fibroblasts (HELFs) via transient transfection of miR-214-3p mimics, inhibitors, or MAP2K3-overexpression plasmids. Cell proliferation was evaluated using the EdU assay, and TGF-β1 secretion was measured by ELISA. SmO exposure induced significant pulmonary fibrosis in mice, accompanied by marked downregulation of miR-214-3p and upregulation of MAP2K3 in lung tissues. Overexpression of miR-214-3p or silencing of MAP2K3 effectively suppressed SmO-induced fibroblast activation, including reduced cell proliferation, decreased expression of α-SMA and Collagen I, and inhibition of p38 MAPK phosphorylation. Notably, ectopic overexpression of MAP2K3 reversed the protective effects conferred by miR-214-3p, confirming a functional rescue. miR-214-3p directly silences MAP2K3, thereby blunting p38 MAPK-driven fibrogenesis after SmO exposure. Our data unveil a miR-214-3p-MAP2K3-p38 MAPK axis that constitutes a readily druggable target for rare-earth-element-induced pulmonary fibrosis. - Source: PubMed
Publication date: 2026/03/08
Sun YingDing RuixiaYin HaijingMa TengBi YannanLi ShengWang LiWang Xiaohui - Forchlorfenuron is a widely used plant cytokinin in Traditional Chinese Medicine and agricultural cultivation to boost resistance, postpone senescence, and increase productivity. However, the improper use of forchlorfenuron results in excessive residues and contamination, raising health and safety concerns. Our research investigated the toxicity of forchlorfenuron on hepatocytes in vitro. Results showed that forchlorfenuron inhibited HepaRG cell viability in a concentration and time-dependent manner. Forchlorfenuron-induced cellular apoptosis and the increased intracellular reactive oxygen species (ROS) indicated the participation of oxidative stress. Molecular docking and network pharmacology data suggested that the hepatotoxicity of forchlorfenuron might involve the MAPK signaling pathway. After 24 h of forchlorfenuron exposure, the P38-MAP kinase, upstream kinases MKK3, and the transcription factor ATF2 were maximally activated. Apoptosis induced by forchlorfenuron was significantly reduced by pretreatment with the P38 inhibitor SB203580. These findings implicated that HepaRG hepatocyte injuries were generated by forchlorfenuron through the induction of cellular apoptosis via the MKK3/P38/ATF2 pathway. Forchlorfenuron application should be closely managed to prevent potential liver damage. - Source: PubMed
Publication date: 2026/02/26
Zhang YunqiLuo YunChe XiaoyangDai ZiruSun XiaoSun Xiaobo - Epigenetic inhibitors exhibit powerful antiproliferative and anticancer activities. However, cellular responses to small-molecule epigenetic inhibition are heterogeneous and dependent on factors such as the genetic background and metabolic state of cells, as well as on-/off-target engagement of individual small-molecule compounds. The molecular study of the extent of this heterogeneity often measures changes in a single cell line. To more comprehensively profile the effects of small-molecule perturbations and their influence on heterogeneous cellular responses, we present a molecular resource based on the quantification of chromatin, proteome, and transcriptome remodeling due to histone deacetylase inhibitors (HDACi) in non-isogenic cell lines. Through quantitative molecular profiling of 10,621 proteins, these data reveal coordinated molecular remodeling of HDACi treated cancer cells. HDACi-regulated proteins differ greatly across cell lines with consistent (JUN, MAP2K3, CDKN1A) and divergent (CCND3, ASF1B, BRD7) cell-state effectors. Together these data provide valuable insight into cell-type driven and heterogeneous responses that must be taken into consideration when monitoring molecular perturbations in culture models. We have also built a web interface for the extensive amount of data to allow users to explore the data as a resource for understanding chemical perturbation of diverse cell types. - Source: PubMed
Publication date: 2026/01/28
Lin ChuweiSniezek Catherine MMcGann Christopher DKarki RashmiGiglio Ross MGarcia Benjamin AMcFaline-Figueroa José LSchweppe Devin K