Ask about this productRelated genes to: MAPKAPK2 antibody
- Gene:
- MAPKAPK2 NIH gene
- Name:
- MAPK activated protein kinase 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-03-26
- Date modifiied:
- 2019-04-12
Related products to: MAPKAPK2 antibody
Related articles to: MAPKAPK2 antibody
- MAPKAPK2 is a promising therapeutic target in numerous diseases. However, many MAPKAPK2 inhibitors are plagued by low solubility and permeability, and none have advanced through clinical trials. New computational methods utilizing deep learning can speed up inhibitor identification. This study aims to develop and validate a novel framework for MAPKAPK2 inhibitor discovery utilizing an ensemble of ten individual models trained on various feature sets. We trained DNN models using 21 molecular featurizers and 28 layer-size settings, and selected ten high-performing feature-architecture combinations to establish the ensemble. We explored various voting methods in conjunction with the ensemble and used the ensemble to generate a ranking of potential MAPKAPK2 inhibitors from an in-house compound set. Potential inhibitors satisfying Lipinski and Veber Rules not containing PAINS structures were selected for enzyme assay testing, and a molecular docking simulation was performed to investigate interactions. The individual model with the highest evaluation metrics was trained on functional-class fingerprints. Meanwhile, the ten-model voting ensemble reported an accuracy of 0.969 on a testing set. One novel MAPKAPK2 inhibitor, S021-0180, was identified out of seven tested with enzyme assays. The molecular docking simulation revealed critical ligand-residue interactions within the binding site. The novel computational framework was successful in identifying a novel MAPKAPK2 inhibitor as a promising inhibitor for further optimization in future studies. The established ensemble can be used to evaluate more compound sets for novel MAPKAPK2 inhibitors. Moreover, we anticipate that this new framework can be applied to all protein kinases for rapid compound screening. - Source: PubMed
Publication date: 2026/09/05
Chen HaydenWu Yi-WenLin Tony EightChen Jun-HongChan Yu-ChengYang Chun-LinYen Shih-ChungHuangFu Wei-ChunPan Shiow-LinHsu Kai-Cheng - Topmouth culter () is highly sensitive to hypoxic conditions, but its regulatory mechanisms remain poorly understood. In this study, were exposed to hypoxia (DO: 0.60 ± 0.05 mg·L) for 0, 2, 4, 6, 12, and 24 h to investigate the gill tissue responses and the underlying regulatory mechanisms. Results showed that gill lamellae of exhibited distortion and thickening under hypoxic stress for 2-6 h. Between 12 and 24 h of hypoxia, the gill tissue exhibited changes characterized by sinusoidal dilatation and an increased number of red blood cells. Interestingly, the apoptosis rates significantly increased in all experimental groups in response to the hypoxic environment. The plasma glucose (Glu) level increased rapidly at the early stage and then gradually declined. The total protein (TP) level showed a slight elevation. Meanwhile, low-density lipoprotein (LDL) and high-density lipoprotein (HDL) exhibited sustained increases. Hypoxia stress may induce a metabolic transition from early reliance on glucose for energy to later reliance on lipid metabolism. SOD activity gradually increased under hypoxia, while MDA content exhibited an overall upward trend. Oxidative stress-related genes (, , , ) were significantly upregulated to enhance antioxidant capacity during the early phase of hypoxic stress. However, during the late phase of hypoxia, the expression of these genes was significantly downregulated. In conclusion, this study offers a new theoretical basis for gill tolerance remodeling and molecular regulation in under acute hypoxic stress. - Source: PubMed
Publication date: 2026/07/24
Tang JinmeiZhao HualiZhang HaoKoroma KabbaFang Di'an - Inflammation is essential for host defense, but, when dysregulated, it contributes to tissue damage and chronic disease. MicroRNA-146a (miR-146a) is a well-recognized negative regulator of inflammatory signaling, primarily through suppression of the NF-κB pathway; however, its broader proteomic impact under inflammatory conditions remains incompletely defined. In this study, we overexpressed an miR-146a mimic in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages and applied quantitative mass spectrometry to characterize global protein abundance changes. Functional overexpression was supported by reduced mRNA abundance of the established miR-146a targets TRAF6 and IRAK1 under LPS-stimulated conditions. Proteomic analysis identified 1232 proteins showing differential abundance under the predefined exploratory criteria, including proteins related to NF-κB activity, inflammasome components, nitric oxide synthesis, and IL-6-associated pathways. Proteins linked to interferon-related signaling were also altered. Targeted validation by quantitative RT-PCR and parallel reaction monitoring supported changes in selected inflammatory mediators, including PTGS2, NOS2, MAPKAPK2, and IRF3. Functionally, miR-146a overexpression was associated with reduced LPS-induced nitric oxide and IL-6 production. Together, these findings provide an exploratory proteomic overview of pathways associated with miR-146a overexpression in activated macrophages and suggest that miR-146a is associated with modulation of multiple inflammatory signaling networks under inflammatory conditions. - Source: PubMed
Publication date: 2026/07/22
Tangwattanachuleeporn MarutSrichaimongkol AunyamonMakjaroen JiradejVirakul SitaNanthawong SaharatSun H SunnyDewi Ni Nyoman AyuPalaga TanapatWongsurawat ThidathipLeelahavanichkul AsadaSomparn Poorichaya - Influenza, an acute respiratory infectious disease caused by the influenza virus, remains a significant challenge for prevention and treatment due to rapid viral mutation and high pathogenicity. Traditional Chinese Medicine (TCM), including Shuangyu Granule (SYKL), has demonstrated efficacy in managing influenza. This study aimed to systematically identify the chemical components of SYKL in vitro and its absorbed constituents in vivo, and to preliminarily explore its potential mechanism in regulating influenza-related immune inflammation. UPLC-Orbitrap-MS/MS and GC-MS were used to characterize SYKL's chemical profile, identifying 148 in vitro components and 21 prototype absorbed blood components. Network target analysis, integrated with single-cell RNA sequencing (scRNA-seq) data from influenza patients, predicted that the absorbed components may target multiple immune-inflammatory regulatory genes across various immune cell types. Molecular docking suggested favorable predicted binding potential between these components and target proteins. Experimental validation using poly(I:C)-induced inflammatory models in both RAW264.7 macrophages and mouse bone marrow-derived macrophages (BMDMs) showed that the absorbed components-loganic acid, 8-epiloganic acid, calycosin, atractylodin, eucalyptol, secoxyloganin, and paeoniflorin-significantly reduced mRNA expression of immune-inflammatory genes (DUSP6, MAPKAPK2, NOD2) and inhibited secretion of TNF-α, IL-6, IL-8, and NO. These findings suggest that SYKL may alleviate influenza-associated inflammation through multi-component, multi-cell, and multi-target pathways, highlighting its potential in modulating excessive immune responses in influenza. - Source: PubMed
Publication date: 2026/07/27
Sun LingJiang ZhiTaoChen YingHan MingShuLv YaoZhongLi LiangZhang XinZhuangCao LiangWang TuanJieWang ZhenZhongXiao Wei - Memory T-cell inflation is a distinctive immunological phenomenon observed during persistent viral infections such as cytomegalovirus (CMV). Unlike conventional memory T-cell responses, which contract after infection resolution, a subset of CMV-specific T cells undergoes a progressive and sustained expansion, termed "inflation", which is thought to be critical for long-term immune surveillance. The molecular mechanisms that govern memory T-cell inflation remain incompletely understood, yet they are pivotal for understanding immune persistence and designing strategies against chronic viral infections. In this study, we investigated the role of MAPK-activated protein kinase 2 (MK2), a key downstream effector of p38 MAPK signaling, in regulating T-cell responses during murine CMV (MCMV) infection. Using MK2 knockout (MK2-KO) mice, we demonstrate that MK2 deficiency alters the dynamics of MCMV-specific CD8+ T-cell responses without impairing viral control or tissue replication. MK2 deficiency led to a reduction in noninflationary MCMV-specific CD8+ T cells during acute infection, followed by enhanced expansion of inflationary CD8+ T-cell subsets during latent infection. Furthermore, MK2-KO mice exhibited impaired effector differentiation, as evidenced by decreased expression of the terminal differentiation marker KLRG1 on MCMV-specific CD8+ T cells. Collectively, these findings identify MK2 as an important regulator of CD8+ T-cell magnitude, kinetics, and phenotype during both acute and latent MCMV infection. By demonstrating a role of MK2 in the regulation of memory T-cell inflation, this study provides new mechanistic insight into immune regulation with implications for vaccination, chronic infection, and immune aging. - Source: PubMed
Panagioti EleniYu XueyangKong Yi WenMacakova KristinaMercado Noe BLawler Sean EdwardYaffe Michael BCook Charles H