Ask about this productRelated genes to: AGPAT2 antibody
- Gene:
- AGPAT2 NIH gene
- Name:
- 1-acylglycerol-3-phosphate O-acyltransferase 2
- Previous symbol:
- BSCL
- Synonyms:
- LPAAT-beta
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-07
- Date modifiied:
- 2019-04-17
Related products to: AGPAT2 antibody
Related articles to: AGPAT2 antibody
- This study explores the links between palmitoylation-related genes and the progression of osteoarthritis (OA) and its downstream regulatory mechanism. - Source: PubMed
Publication date: 2026/04/08
Di JingkaiGuo ZijianChen TingtingHe JinsongQin YingdaWang FeidaXiang Chuan - Congenital generalized lipodystrophy (CGL) type 1, caused by mutations in 1-acylglycerol-3-phosphate O-acyltransferase 2 (AGPAT2), is characterized by near-total absence of adipose tissue and severe metabolic disturbances, including hepatic steatosis, insulin resistance, and hypertriglyceridemia. Although AGPAT2's enzymatic function in lysophosphatidic acid acylation during glycerolipid biosynthesis is well characterized, the molecular mechanisms driving disease pathogenesis remain incompletely understood. In this study, significant up-regulation of glycerol-3-phosphate acyltransferase 3 (GPAT3), in both embryonic fibroblasts and liver tissue from AGPAT2-deficient mice, was identified. Through generation of Agpat2/Gpat3 double-knockout mice, it was demonstrated that GPAT3 ablation leads to multiple metabolic improvements: enhanced survival rates, partial preservation of adipose tissue (with more pronounced effects in brown than white adipose depots), marked attenuation of hepatic steatosis accompanied by reduced inflammation and fibrosis, and amelioration of hyperglycemia and hyperinsulinemia. Neonatal analyses demonstrated that GPAT3 deletion delayed adipose tissue degeneration while markedly decreasing macrophage infiltration (F4/80 cells) and apoptotic signaling (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive cells). Ultrastructural examination revealed improved adipocyte morphology with normalized organelle architecture. These results identify GPAT3 as a key metabolic regulator in AGPAT2 deficiency, demonstrating that its inhibition partially restores adipose tissue and liver function. The conserved benefits of GPAT3 deficiency in both CGL1/AGPAT2 and CGL2/Seipin models highlight GPAT3 as a promising therapeutic target for congenital lipodystrophies. - Source: PubMed
Publication date: 2026/03/23
Liang ChenxiChen XinWang XiaoweiTang JinyeLiu ZiweiLi JiaxuanYan HaiyiWu JinQiu LiwenGu JingwenDou YaqianZhao XiaohuiYang HongyuanGao Mingming - Berardinelli-Seip syndrome, also known as congenital generalized lipodystrophy (CGL), is a rare genetic disorder characterized by lipoatrophy, acromegaloid features, hyperinsulinemia, hypertriglyceridemia, and hepatic steatosis. With estimated prevalence 1 in every 10,000,000 births, CGL challenges medical specialists to seek better ways for early diagnosis of the disease. Despite its rarity, the condition is associated with severe metabolic and cardiovascular complications, leading to significant morbidity and reduced life expectancy. Advances in molecular genetics have identified mutations in AGPAT2, BSCL2, CAV1, and PTRF, which provide important insights into adipose tissue biology and systemic metabolism. Early recognition and genetic confirmation are crucial to initiate timely interventions, including lifestyle modification, insulin sensitizers, and lipid-lowering therapies including metreleptin therapy in indicated cases. Two illustrative cases are presented, reflecting our experience with the clinical variability, genetic findings, and therapeutic strategies in CGL as well as highlighting the importance of comprehensive care and emerging therapies. - Source: PubMed
Yordanova Savelia GavrailovaTodorova ZdravkaGateva AntoanetaKaramfilova VeraArchinkova MargaritaKamenov ZdravkoAssyov Yavor - Sheep () tail fat serves as a crucial energy reserve for adapting to harsh environments. However, excessive deposition can reduce farming efficiency and product quality. Elucidating the regulatory mechanisms of tail fat deposition is of great significance for genetic improvement in sheep. - Source: PubMed
Publication date: 2026/01/30
Gao LeiZhang YunyunZhang YiyuanPeng WeifengZhang ZhenliangLiu YuchengWang JingjingWan PengchengZhao Zongsheng - Adipocyte differentiation involves a metabolic transition from oxidative phosphorylation (OXPHOS) to aerobic glycolysis, allowing preadipocytes to meet the biosynthetic and energetic demands of maturation. Here, we show that nuclear myosin 1 (NM1), a chromatin-associated actomyosin motor, known to control transcription and chromatin accessibility, is required for metabolic homeostasis during adipocyte differentiation. Integrated ATAC-seq and RNA-seq profiling of NM1-deficient mouse embryonic fibroblasts (MEFs) revealed coordinated downregulation of key adipogenic and lipid-droplet machinery genes like Cebpa, Plin2, Abhd5, Agpat2, Pink1, and altered enhancer accessibility near adipogenesis-linked transcription factors (TFs) such as Klf6, Foxo3, Smad5, and Gata4. NM1 knockout (KO) mesenchymal stem cells (MSCs) exhibited impaired differentiation potential despite enlarged adipocyte morphology. In vivo, NM1-deficient mice developed progressive visceral obesity, accompanied by transcriptional reprogramming in epididymal white adipose tissue (eWAT), including repression of mitochondrial and adipogenic pathways and activation of inflammatory networks driven by IFNG, IL33, and TNF. Cross-species network analysis highlighted conserved regulatory architecture centered on MYO1C, implicating NM1/MYO1C as key chromatin-level regulators of adipose remodeling. - Source: PubMed
Publication date: 2026/02/26
Khalaji SamiraVenit TomasLukáčová ZuzanaFambri ValentinaShrestha RahulKaluarachchi SachinBoitet MaylisFagny MaudSaldi GiuseppePercipalle Piergiorgio