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
- Coronary artery disease (CAD), a chronic progressive inflammatory cardiovascular disorder and leading global cause of mortality, imposes a substantial worldwide economic burden. Identifying lipid metabolism-related genes linked to CAD is crucial for deepening our understanding of the disease's pathogenesis and discovering novel therapeutic targets. A total of 700 differentially expressed genes associated with CAD were determined by comparing CAD patients and healthy controls in the GSE250283 dataset. A positive relationship between lipid exposure and CAD was revealed by implementing a 2-sample Mendelian randomization analysis using genome-wide association studies data on lipid metabolism exposures and CAD outcomes. Further Mendelian randomization analysis, employing expression quantitative trait loci data from the identified differentially expressed genes as exposures and intersecting results with the Kyoto Encyclopedia of Genes and Genomes lipid metabolism pathway, identified 19 key genes exhibiting both lipid regulatory characteristics and reliable causal associations with CAD. Finally, 5 biomarker genes (SCP2, TNFAIP8, HMGCR, AGPAT3, and MAPKAPK2) were selected from the key genes by implementing 4 machine learning algorithms, and the developed nomogram incorporating these biomarkers demonstrated superior predictive accuracy for CAD risk stratification. The identification of these 5 genes as causal lipid metabolism biomarkers of CAD offers novel insights with high clinical potential, providing valuable targets for the management and treatment of CAD. - Source: PubMed
Bure QiSun WenjinWang LujiaoZhang XinShuang Lian - Trigeminal neuralgia (TN) is a neuropathic pain disorder with a marked female predominance. While transcriptional changes in TN are documented, the translational and post-translational landscapes-specifically protein abundance and phosphorylation states-within the trigeminal ganglion (TG) remain largely unexplored. Understanding these layers is essential to deciphering the mechanisms behind the disease's sexual dimorphism. - Source: PubMed
Publication date: 2026/03/03
Zhai XiaojieLin XianghongZhang LinlinRen YuxuanMiao HeMiao MengmengChen YijunZhang YiweiHuang Changshun - Cabozantinib is a multi-target tyrosine kinase inhibitor used in renal cell carcinoma (RCC), yet the exposure-dependent remodeling of phosphorylation networks under short-term chronic treatment remains insufficiently defined. This study applied quantitative phosphoproteomics to delineate remodeling programs induced by acute and chronic cabozantinib exposure and to examine cellular features within the same signaling background. - Source: PubMed
Chen Shao-KuanWang Yen-ChiehHsieh Yu-HengHuang Chi-JungKu Wei-Chi - Esophageal squamous cell carcinoma (ESCC) remains a leading cause of cancer-related mortality worldwide. Long non-coding RNAs (lncRNAs) play essential roles in ESCC progression. In this study, we profiled lncRNA expression in ESCC cells following serum deprivation and identified LHFPL3-AS2 as a serum starvation-inducible, oncogenic lncRNA. LHFPL3-AS2 could promote invasion and metastasis of ESCC cells in vitro and in vivo. Mechanistically, LHFPL3-AS2 directly binds to hnRNPA0 protein, enhances its interaction with its kinase MAPKAP-K2 (MK2), and promotes MK2-mediated phosphorylation of hnRNPA0 at serine 84. The phosphorylated hnRNPA0 binds to several oncogenic transcripts, such as the BMP7 mRNAs, stabilizes these mRNAs and elevates their expression in ESCC cells. Importantly, LHFPL3-AS2 enhances polarization of macrophages toward an immunosuppressive M2 phenotype via upregulating BMP7 secretion by cancer cells, thereby facilitating tumor immune evasion and ESCC progression. Overall, our study identified a previously unappreciated LHFPL3-AS2-MK2-hnRNPA0-BMP7 axis in cancer progression under serum starvation conditions and provides mechanistic insight for ESCC. - Source: PubMed
Publication date: 2026/02/16
Xu YuanZhang ZiqiYang YantingLi MinxinWang HaipengZhang LongWang ShouyuRen ChuanliZhang NashaLi ZengjunYang Ming - The kinase MAPKAPK2 regulates cell survival, proliferation, and death, and is upregulated in colorectal carcinoma (CRC) where it is associated with tumor growth and progression. However, how it regulates tumor progression in conjunction with other signaling pathways, such as MEK/ERK, remains elusive. Solid tumors are often subjected to metabolic stress, notably glucose deprivation. Here, we demonstrate that MAPKAPK2 protein levels in CRC regulate cell fate decision during stress conditions, such as glucose deprivation and therapeutic treatment. While MAPKAPK2 expression is a limiting factor for CRC growth in vitro, depleting MAPKAPK2 or inhibiting its activity pharmacologically provides a survival advantage to CRC cells under glucose limiting conditions. Subjecting CRC cells to low glucose resulted in an ERK1/2-mediated decline in MAPKAPK2 to promote survival. Additionally, cells with reduced MAPKAPK2 activity were less sensitive to trametinib under glucose limiting conditions. Utilizing transcriptomic profiling, we found that glucose deprivation and MAPKAPK2 depletion activate pathways associated with survival during metabolic stress. This relationship was also observed in CRC patients (TCGA), where tumors with low MAPKAPK2 expression had higher ERK1/2 activation and upregulated stress-induced pathways, leading to poor survival. Finally, MAPKAPK2 modulated growth of CRC organoids, subcutaneous tumors, and patient-derived xenografts (PDX), and reduced MAPKAPK2 levels decreased efficacy of trametinib, in vitro and in vivo. Overall, this study identifies an interrelationship between MEK/ERK and p38/MAPKAPK2 signaling pathways during glucose deprivation to support cell survival and features MAPKAPK2 loss as a possible mechanism leading to reduced efficacy of trametinib-based anticancer therapy and poor patient outcomes in CRC. - Source: PubMed
Publication date: 2026/02/09
Kumari NitiChen XuBaldwin Amber MClemons Kristin IEl-Harakeh MohammadCalisto Lilian EKumar BalawantZhang QiaoqiaoMin JiangXiao BinSingh Amar BWang BinNorth Brian J