APOC3 ELISA kit
- Known as:
- APOC3 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-APOC3-Ra
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- APOC3 ELISA kit
Related genes to: APOC3 ELISA kit
- Gene:
- APOC3 NIH gene
- Name:
- apolipoprotein C3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-04-26
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- Reducing plasma levels of low-density lipoprotein cholesterol (LDL-C) is the cornerstone in the prevention of coronary artery disease (CAD) but may also increase risk of type 2 diabetes (T2D). A comprehensive examination of the genetic evidence of T2D related side-effects of all current lipid-modifying drugs, including those in development, has not yet been performed. - Source: PubMed
Publication date: 2026/05/14
Chen ZekaiTriatin Rima DLuo LiSnieder HaroldSchmidt A FloriaanDitmarsch MarcKastelein John J PDullaart Robin P FKuivenhoven Jan AlbertThio Chris H L - Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating condition associated with approximately 30% mortality and 20% severe disability among survivors. Delayed cerebral ischemia due to cerebral vasospasm and hydrocephalus significantly contribute to poor neurological outcomes. Currently, reliable biomarkers for early prediction of these complications remain lacking. In this study, 63 patients with a mean age of 59.7 ± 11.53 years were enrolled. Functional outcomes were assessed by the modified Rankin Scale (mRS). Cerebrospinal fluid (CSF) samples were obtained through lumbar drainage (LD) or external ventricular drainage (EVD) and analyzed by ELISA. The predictive value of biomarkers was evaluated using receiver operating characteristic (ROC) curve analysis. Elevated Apolipoprotein C-III (ApoC3) levels in CSF of aSAH patients were observed. Furthermore, increased ApoC3 concentrations were significantly associated with poor prognosis and an elevated risk of severe complications. At an optimal cutoff value of 4,463 ng/mL, patients with high ApoC3 levels exhibited significantly worse 3-month functional outcomes and a higher incidence of delayed cerebral ischemia and hydrocephalus. Monitoring ApoC3 levels in CSF may be beneficial for predicting complications such as delayed cerebral ischemia and hydrocephalus in patients with aSAH. - Source: PubMed
Publication date: 2026/04/17
Tong BinWang JunjieChen JiaruiZhang QiaXu ZhouhanYang KaichuangChen Xiaomin - Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by hepatic triglyceride accumulation in the setting of obesity and insulin resistance. Although apolipoprotein C-III (APOC3) is a well-established regulator of plasma triglyceride metabolism, its hepatocyte-intrinsic role in intracellular lipid accumulation remains unclear. In this study, we investigated whether APOC3 contributes to hepatocellular triglyceride synthesis during early metabolic dysfunction. In 6-week-old db/db mice, early hepatic lipid accumulation was observed without detectable fibrosis. Transcriptomic profiling identified as an upregulated gene associated with lipid metabolic pathways, and its hepatic upregulation was confirmed at both mRNA and protein levels. Gain- and loss-of-function experiments in HepG2 cells demonstrated that APOC3 overexpression significantly increased intracellular triglyceride content, whereas APOC3 knockdown reduced triglyceride accumulation. Mechanistically, APOC3 selectively regulated diacylglycerol acyltransferase 2 (DGAT2), which catalyzes the final step of triglyceride synthesis, without significantly affecting major lipogenic transcription factors. Furthermore, under de novo lipogenesis-inducing conditions triggered by the liver X receptor agonist T0901317 and insulin, APOC3 markedly amplified DGAT2 expression and triglyceride accumulation. Collectively, these findings suggest a hepatocyte-intrinsic role for APOC3 in promoting triglyceride accumulation through DGAT2-dependent mechanisms. The APOC3-DGAT2 axis may represent a relevant pathway contributing to hepatic lipid accumulation in metabolic liver disease. - Source: PubMed
Publication date: 2026/04/20
Nguyen Thi NhiKim Hye-JeongShim Hye MinKang JunhoHa Eun YoungCho HochanPark Jae-Hyung - Porcine epidemic diarrhea (PED) is a severe viral disease caused by the porcine epidemic diarrhea virus (PEDV), leading to huge economic losses in the swine industry. Identifying therapeutic targets has long been a critical challenge in preventing and controlling PED through nutritional interventions. In the present study, 100 seven-day-old crossbred (Duroc × Landrace × Large White) healthy piglets from seven independent trials were selected for the experiment. The transcriptomics, proteomics, and metabolomics analyses were conducted on the small intestine and blood of piglets infected with PEDV, and the combined multiple batches of data were subsequently subjected to integrated analysis. Our findings revealed that PEDV infection significantly affected intestinal cell metabolism, especially lipid metabolism. Among those, sphingolipid and lysophospholipid metabolism could be potential pathways for preventive and therapeutic interventions. Additionally, retinol metabolism, mineral absorption, amino acid metabolism, and pyrimidine metabolism were remarkably altered following PEDV infection. Subsequently, candidate hub genes involved in the core pathways, such as apolipoprotein C3 (APOC3), cytochrome P450 family 3 subfamily A member 22 (CYP3A22), and intestinal alkaline sphingomyelinase (ENPP7), were identified and validated. In conclusion, the present study suggests that PEDV infection leads to the reprogramming of enterocyte lipid metabolism. Furthermore, manipulating lipid metabolism may influence the outcome of viral infection, highlighting potential targets for preventive and therapeutic interventions in managing viral infections. - Source: PubMed
Publication date: 2026/04/30
Wu MengjunZhang QianShi XintaoLi PengSong ZhuanLi ZhonghuaZhang YanyanWang LeiZhao DiWu TaoYi DanHou Yongqing - Small dense low-density lipoprotein (sdLDL) is a highly atherogenic LDL subclass associated with cardiovascular disease (CVD). While type 1 diabetes confers increased cardiovascular risk despite adequate glycemic control, the role of sdLDL and its regulators remains unclear. - Source: PubMed
Publication date: 2026/04/07
Sardà HelenaSolé ArnauColom CristinaBorràs CarlaCarreras GemmaBenítez SoniaMiñambres InkaEscolà-Gil Joan CarlesSánchez-Quesada José LuisPérez Antonio