Human Apolipoprotein C3 ELISA , APOC3
- Known as:
- Human Apolipoprotein C3 Enzyme-linked immunosorbent assay test , APOC3
- Catalog number:
- E01A0516
- Product Quantity:
- 96 Tests/kit
- Category:
- -
- Supplier:
- BGene
- Gene target:
- Human Apolipoprotein C3 ELISA APOC3
Related genes to: Human Apolipoprotein C3 ELISA , APOC3
- 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
Related products to: Human Apolipoprotein C3 ELISA , APOC3
Related articles to: Human Apolipoprotein C3 ELISA , APOC3
- Elevated cholesterol levels are associated with the risk of the most socially significant cardiovascular diseases, such as atherosclerosis, ischemic heart disease, and myocardial infarction. - Source: PubMed
Publication date: 2026/06/02
Mamchur AleksandraBruttan MariaDaniel VeronikaKashtanova DariaZelenova ElenaDzhumaniiazova IrinaIvanov MikhailMatkava LorenaBlinova OlgaMitrofanov SergeyGolubnikova LiliyaKumar NaianaMaralova EkaterinaShingaliev AndreyEzhov MaratMeshkov AlekseyChubykina UlianaPogorelova OlgaTripoten MariiaBalahonova TatyanaViskova AlexandraKomarova MadinaGurtsiev TimurGomyranova NataliaVorobeva YuliaHotuleva AnastasiaKolyaskina MariaYudin VladimirMakarov ValentinKeskinov AntonKuzmina LyudmilaBoytsov SergeyYudin SergeySkvortsova Veronika - Plozasiran, a hepatocyte-targeted siRNA against apolipoprotein C-III, has demonstrated substantial reductions in triglycerides (TGs) and related atherogenic lipoproteins across a spectrum of hypertriglyceridemia (HTG), leading to its approval for familial chylomicronemia syndrome in the United States, and subsequently in Canada and China. Long-term data suggest maintenance of these effects beyond the blinded treatment periods, supporting further evaluation of plozasiran across a broad spectrum of HTG. - Source: PubMed
Publication date: 2026/03/24
Ballantyne Christie MBaass AlexisRosenson Robert SHegele Robert ANicholls Stephen JVasas SzilardClifton PeterLucas Kathryn JPall DenesZhou RongLeeper Nicholas JHellawell JenniferAiyer LalithaWatts Gerald FGaudet Daniel - - Source: PubMed
Publication date: 2026/03/24
Shapiro Michael DNasir Khuram - Metabolic syndrome involves several lipid-related genes, including apolipoprotein A5 (APOA5), lipoprotein lipase (LPL), and cholesteryl ester transfer protein (CETP). Although individual SNP susceptibility has been reported, gene-gene interactions remain underexplored. To address this gap, we apply many-objective multifactor dimensionality reduction (MaODR)-previously developed by our group-to detect gene‒gene interactions in unbalanced newly identified MetS and non-MetS subjects. - Source: PubMed
Publication date: 2026/06/09
Lin Yu-DaLuo Kuei-HauChuang Li-YehChuang Hung-YiYang Cheng-Hong - Type 1 diabetes and type 2 diabetes are associated with an increased risk of atherosclerotic cardiovascular disease (ASCVD), manifested as myocardial infarction, ischemic stroke, and peripheral artery disease. The increased ASCVD risk in diabetes cannot be fully explained by traditional risk factors. This review highlights the dysregulation of TRLs (triglyceride-rich lipoproteins; VLDL [very low-density lipoprotein] and chylomicrons), and their remnants, as contributors to ASCVD risk in diabetes by examining 6 typical clinical cases integrated with mechanistic data obtained in preclinical models. Type 2 diabetes is often associated with insulin resistance and increased hepatic secretion of VLDL particles, which are enlarged by an increased lipid load, increased intestinal secretion of chylomicrons, and reduced hepatic clearance of both VLDL and chylomicron remnants. The increased levels of TRLs in turn contribute to the predominance of smaller, denser LDL (low-density lipoprotein) particles and smaller cholesterol-depleted HDL (high-density lipoprotein) particles compared with people without diabetes. When type 2 diabetes occurs in individuals with genetic variants causing altered function of proteins stimulating TRL clearance (, or ) or suppressing TRL clearance (), the result is a compounded accumulation of TRLs and their remnants in plasma and an associated increased ASCVD risk. VLDL secretion is usually unaltered in individuals with well-controlled type 1 diabetes, but ASCVD risk is increased when insulin resistance and defects in TRL clearance are also present. Mechanistically, TRLs enhance ASCVD risk at least in part by exacerbating local vascular inflammation caused by the accumulation of free cholesterol and triglyceride lipolysis products. Because cardiovascular outcome trials targeting triglyceride levels to date have been mostly futile, the field is now focused on trials targeting proteins involved in TRL clearance. Carefully determining inclusion and exclusion criteria for such trials will be critical for advancing our understanding of how to better prevent ASCVD in individuals living with diabetes. - Source: PubMed
Publication date: 2026/06/04
Ginsberg Henry NBornfeldt Karin E