Polyclonal Rabbit AGPAT3 Antibody
- Known as:
- Polyclonal Rabbit AGPAT3 Antibody
- Catalog number:
- KA0133
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit AGPAT3 Antibody
Related genes to: Polyclonal Rabbit AGPAT3 Antibody
- Gene:
- AGPAT3 NIH gene
- Name:
- 1-acylglycerol-3-phosphate O-acyltransferase 3
- Previous symbol:
- -
- Synonyms:
- LPAAT-gamma, LPAAT3
- Chromosome:
- 21q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-16
- Date modifiied:
- 2019-03-26
Related products to: Polyclonal Rabbit AGPAT3 Antibody
Related articles to: Polyclonal Rabbit AGPAT3 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 - Ferroptosis plays a critical role in immune regulation and tumor microenvironment remodeling. However, its therapeutic potential in enhancing immune checkpoint inhibitor (ICI) efficacy remains incompletely understood and warrants further investigation. - Source: PubMed
Publication date: 2026/03/10
Liu ChuanHu ChuanCheng JinlinXin DuanfengJin SujieTian WeihongLi ShanJin YuzhiLiu YuWu WeiHao ShuqiangRen HuiDai XiaomengLiu LuluRuan JianFang WeijiaBao XuanwenXin ShanZhao Peng - Recent studies have shown glycerolipid metabolism played an essential role in multiple tumors, however, its function in osteosarcoma is unclear. This study aimed to explore the role of glycerolipid metabolism in osteosarcoma. - Source: PubMed
Publication date: 2025/12/30
Su ShenghuiZeng YuChen JiaxinDong Xieping - Stroke remains a major global health challenge due to its high mortality and significant socioeconomic burden. Despite advances in clinical management, effective diagnostic tools and therapeutic strategies remain limited. This study aimed to identify and expand the repertoire of biomarkers of damage and repair that could serve as potential diagnostic and prognostic tools across post-stroke phases. Twenty-three male wild-type mice were assigned according to three longitudinal time points to control pre-stroke, 24-hour acute, and 35-day chronic post-stroke groups. Ischemic injury was induced via a 30-minute middle cerebral artery occlusion Koizumi method. Magnetic resonance imaging and neurological scoring were used to assess lesion size and functional deficit acutely, as well as structural and functional recovery during the chronic phase. Proteomic profiling of the ipsilateral and contralateral cortices was performed using data-independent acquisition (DIA)-based MS method. Statistical analysis revealed 74 differentially expressed proteins showing significant temporal changes in expression, which were classified into four temporal expression clusters: acutely and chronically upregulated, acutely upregulated and chronically downregulated, acutely downregulated and chronically upregulated, and acutely and chronically downregulated. Gene ontology analysis identified 47 affected biological processes, including synaptic signaling, immune response, cell-cell communication, cytoskeletal organization, and proliferation. Thirteen proteins previously not associated with stroke pathophysiology were identified, including 10 from the ipsilateral cortex (Dbi, Cpne3, Dnm2, Eef1a1, Taldo1, Pgls, Gnb5, Phf24, Ctsz, Capg) and 3 from the contralateral cortex (Agpat3, Cacng8, Endod). The identified biomarkers provide novel molecular insights into post-stroke energy metabolism, neuroinflammation, and cellular remodeling, highlighting potential targets for further intervention. - Source: PubMed
Publication date: 2025/12/04
Hamer DominikButorac AnaPetrinec DanielaBerecki MonikaMendes Vera MManadas BrunoKelava VanjaK Hackenberger BranimirGlasnović AntonLovrić MarijaGajović SrećkoDobrivojević Radmilović Marina - Although polyunsaturated phospholipids are vital for cellular functions, their overaccumulation renders cells vulnerable to ferroptosis. It remains unclear how cells exposed to excess polyunsaturated fatty acids (PUFAs) prevent their over-incorporation into phospholipids. Here, we identified a mechanism by which ubiquitin regulatory X domain-containing protein 8 (UBXD8), a fatty acid (FA)-interacting protein, prevents overaccumulation of phospholipids containing docosahexaenoate (DHA), one of the most abundant PUFAs in mammalian cells. UBXD8 binds to and activates 1-acylglycerol-3-phosphate O-acyltransferase 3 (AGPAT3), which specifically incorporates DHA into phospholipids. Thus, cultured cells and mouse livers deficient in UBXD8 were resistant to ferroptosis because of reduced production of DHA-containing phospholipids. Excess unsaturated FAs, including DHA, through their interaction with UBXD8, disrupt the UBXD8/AGPAT3 complex, thereby inhibiting AGPAT3-catalyzed synthesis of DHA-containing phospholipids. This FA-sensing mechanism prevents overaccumulation of DHA-containing phospholipids in cells exposed to excess DHA, thus reducing the ferroptotic potency of DHA, a property that might contribute to the health benefits of this ω-3 PUFA. - Source: PubMed
Publication date: 2025/09/10
Deng YaqinVale GoncaloLiang YonggangCui ShaojieXu ShimengMcDonald Jeffrey GYe Jin