Ask about this productRelated genes to: DGKA antibody
- Gene:
- DGKA NIH gene
- Name:
- diacylglycerol kinase alpha
- Previous symbol:
- DAGK, DAGK1
- Synonyms:
- DGK-alpha
- Chromosome:
- 12q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-21
- Date modifiied:
- 2016-10-05
Related products to: DGKA antibody
Related articles to: DGKA antibody
- This study aimed to characterize the genomic features and possible transmission mechanisms of an extensively drug-resistant (XDR) Klebsiella pneumoniae (KP2024). The isolate was recovered from pelvic effusion of a postoperative colon cancer patient in Hebei, China, with a focus on the rare mcr-3.11 gene as well as blaNDM-5 and blaCTX-M-27. - Source: PubMed
Publication date: 2026/05/21
Zhao KaixuanWang WeiMa MingFeng JunhuaQi TianyuWang JiajieHe Jing - Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation and joint destruction. Abnormal T-cell ubiquitination has been implicated in RA pathogenesis, yet its molecular mechanisms remain unclear. - Source: PubMed
Publication date: 2026/03/02
He DantingZhao HaitaoMeng Jinghong - Our previous work revealed that the anti-diarrhea effects of alkaline mineral complex (AMC) water improve metabolism and protect the gut during weaning stress. However, whether AMC water can inhibit viral replication and treat viral diarrhea is unknown. The aim of this study was to explore the ability of AMC water to improve nutrient metabolism and protect against infection. In this study, porcine epidemic diarrhea virus (PEDV) or porcine deltacoronavirus (PDCoV) were used as RNA model viruses, and pseudorabies virus (PRV) or porcine circovirus (PCV) were used as DNA model viruses. Compared with those in the infected group, the virus content in the piglets fed AMC water was reduced, and the intestinal mucosal barrier was repaired. Transcriptome and metabolome results revealed that AMC water regulated lipid metabolism through GPAT2, DGKA, OAT3, FXR, LIPC and SULT2A1. Further studies showed that glycerol, cholesterol, and bilirubin levels increased after viral infection, and that AMC water inhibited cholesterol content and promoted bile acid synthesis. In a cellular model, AMC water reduced lipid droplet density by activating the glycerolipid and bile secretion pathways of the GPAT2/SULT2A1 axis. In addition, knockdown of DGKA and overexpression of SULT2A1 significantly affected the expression of the GPAT2/SULT2A1 axis, and the expression of viral proteins colocalized with lipid droplets was significantly decreased. Our findings suggest that AMC water promotes cholesterol metabolism by activating the GPAT2/SULT2A1 axis, inhibiting viral infection in piglets. This study provides theoretical support for the use of nutritional regulation to inhibit viral infection and provides a new method for antiviral therapy. - Source: PubMed
Publication date: 2026/03/11
Yao XinLi Nuo-WaLiu Ying-YingMalhi Kanwar KumarZhang Tian-TianZhao YangLi Hui-XinLi Jin-Long - To classify differentially methylated CpG sites in periodontitis based on methylation shift direction and location relative to CpG islands. - Source: PubMed
Yoshida KokiSivaramakrishnan GowriAsa'ad Farah - Lung cancer, primarily non-small cell lung cancer (NSCLC), causes the highest cancer-related mortality. Although PD-1/PD-L1 inhibitors have improved survival in advanced NSCLC, they can cause immune-related adverse events. (), a traditional Chinese medicine used for tonifying the lung and kidney and enhancing immune function, has shown therapeutic promise in combination with anti-PD-1 therapy for NSCLC. This study aimed to explore the anti-tumor effect of wild combined with anti-mouse PD-1 in the treatment of Lewis lung adenocarcinoma (LLC) and to elucidate the underlying pharmacodynamic mechanism. LLC mouse model was established via inoculation with LLC cells, followed by treatment with anti-mouse PD-1, , or their combination. The tumor volume, weight, and histological changes of LLC mice were evaluated. The proportions of tumor-infiltrating immune cells in blood and tumors were evaluated by flow cytometry, immunohistochemistry, and immunofluorescence. The underlying mechanisms of the combination of and anti-mouse PD-1 therapy in LLC mice were investigated using an integrated transcriptomics and metabolomics analysis. Treatment with anti-mouse PD-1, , or their combination significantly reduced tumor volume and weight, and attenuated the histopathological changes of LLC mice tumors. Among which, medium-dose combination exhibited significant improvements. Furthermore, the combination of and anti-mouse PD-1 significantly increased the proportion of CD8 T cells and decreased the abundance of Tregs and PMN-MDSCs. Integrated transcriptomics and metabolomics analysis revealed that the combination of and anti-mouse PD-1 can enhance anti-tumor immunity in LLC mice by acting on key immune-related genes, including DGKA, PLA2G7, AMPD1, ATP8B4, and BST1, thereby modulating glycerophospholipid metabolism, the TCA cycle, purine metabolism, and nicotinate-nicotinamide metabolism. Wild combined with anti-mouse PD-1 therapy exerts therapeutic effects against LLC by targeting immune-related genes, modulating associated pathways, increasing the proportion of CD8 T cells, and reducing the infiltration of Tregs and PMN-MDSCs, thereby suppressing tumor growth and inhibiting LLC progression. Further research and clinical studies are needed to validate and expand upon these promising findings. - Source: PubMed
Publication date: 2026/02/04
Liu YingyingGao YaqiSuonanlamao Ma YuananXiao YuancanWei LixinZhou Wenbin