MAPKAPK2 (Phospho-Ser272) Antibody
- Known as:
- MAPKAPK2 (Phospho-Ser272) Antibody
- Catalog number:
- 11806
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- MAPKAPK2 (Phospho-Ser272) Antibody
Related genes to: MAPKAPK2 (Phospho-Ser272) 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 (Phospho-Ser272) Antibody
Related articles to: MAPKAPK2 (Phospho-Ser272) Antibody
- 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 - To identify drug-associated risk signals for neovascular age-related macular degeneration (nAMD) and explore their biological basis. - Source: PubMed
Publication date: 2026/06/01
Sun HongBu FengjiaoXin XiuYan JingchaoHuang Taomin - Vitiligo is an acquired depigmentation disorder caused by melanocyte dysfunction or loss. Oxidative stress is widely considered a key driver to its pathogenesis. Mitogen-activated protein kinase-activated protein kinase 2 (MAPKAPK2) is implicated in oxidative stress responses, although its role in vitiligo remains uncertain. This study intended to investigate whether epigenetic downregulation of MAPKAPK2 aggravates oxidative stress-induced damage in vitiligo melanocytes. - Source: PubMed
Publication date: 2026/04/20
Wang YishanZheng Xiaoyong