APOA5
- Known as:
- APOA5
- Catalog number:
- 001766A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- APOA5
Related genes to: APOA5
- Gene:
- APOA5 NIH gene
- Name:
- apolipoprotein A5
- Previous symbol:
- -
- Synonyms:
- RAP3, APOA-V
- Chromosome:
- 11q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-11
- Date modifiied:
- 2016-10-05
Related products to: APOA5
Related articles to: APOA5
- Metabolic syndrome (MetS) progression involves distinct trajectory states, including newly-developed (ND-MetS), recovered (R-MetS), and persistent MetS (P-MetS), each associated with different cardiovascular disease (CVD) risk profiles. The transition to incident MetS represents a critical window for early dietary intervention, as subclinical metabolic deterioration often precedes clinical recognition. However, the predictive value of dietary quality relative to biochemical and genetic markers within integrated machine learning frameworks remains poorly characterized in longitudinal cohorts. - Source: PubMed
Publication date: 2026/09/22
Yang Hye JeongKim Min JungJang Hyun-JunHur Haeng JeonKim Myung-SunnyPark Sunmin - Polymorphisms in genes involved in obesity-related metabolic pathways are associated with metabolic syndrome (MetS). We hypothesized that variants in FTO, LEP, LEPR, ADRB3, ADIPOQ, TCF7L2, ENPP1, APOA5, PPARG, and CYP11B2 are associated with MetS and obesity-related traits. - Source: PubMed
Publication date: 2026/09/21
Stefani Tamiris Invencioni MoraesHirata Thiago Dominguez CrespoCerda Alvarode Oliveira RaquelDos Santos Marina AparecidaFajardo Cristina MorenoDorea Egídio LimaBernik Márcia Martins SilveiraHirata Mario HiroyukiHirata Rosario Dominguez Crespo - ApolipoproteinA5 (APOA5) plays an important role in regulating plasma triglycerides (TG). Most in vivo data, however, derive from murine models whose lipoprotein metabolism diverges substantially from humans, and no rabbit APOA5 loss-of-function model has previously been described. Microinjection of Cas9 mRNA and two exon-2-targeting sgRNAs into rabbit zygotes yielded 10 founders carrying biallelic loss-of-function alleles, and with an approximately 90% reduction in plasma APOA5 protein. On chow, APOA5 mutant rabbits developed a stable atherogenic dyslipidemia with selectively elevated plasma triglycerides and reduced HDL-cholesterol, both more severe in male than in female mutants. The dyslipidemia was paralleled by accumulation of apolipoprotein B-containing lipoproteins, an enlarged VLDL distribution by fast-protein liquid chromatography, and reduced pre-heparin plasma activities of lipoprotein lipase and hepatic lipase together with correspondingly lower plasma free fatty acids. Mutants also exhibited elevated plasma IL-1β, TNF-α and CCL2 with a selective expansion of circulating monocytes, granulocytes and platelets, indicating a low-grade systemic inflammatory state already under chow conditions. After 8 weeks on a high-fat, cholesterol-enriched diet, mutants developed severe combined dyslipidemia, extensive aortic atherosclerosis with macrophage- and smooth-muscle-rich plaques, and marked hepatic steatosis. In conclusion, biallelic disruption of rabbit APOA5 produces a translationally relevant phenotype that recapitulates principal features of human APOA5 deficiency. The APOA5 mutant rabbit thus provides a tractable large-animal platform for studying residual cardiovascular risk and for evaluating emerging triglyceride-lowering therapeutics. - Source: PubMed
Publication date: 2026/09/21
Zha YiwenFeng LinZhang TingYan KunningWang XingyiCheng YongLiang Jingyan - This study aimed to evaluate the clinical and functional impact of a novel apolipoprotein A5 (ApoA5) variant by assessing lipoprotein lipase (LPL) activity. - Source: PubMed
Publication date: 2026/09/10
Gutiérrez JohnayroCastaño PabloMonsalve ClaudiaLópez NestorToquica Fernando RiveraMora EdwinArmijos Jessica CristinaLores JulianaArenas Henry MauricioGiraldo Germán CamiloSánchez DianaAgudelo NataliaFariña GregorioBerg GabrielaNogueira Juan Patricio - - Source: PubMed
Publication date: 2026/08/23
Liu Yu-LinXiang ZhuoZhang Bo-YaZou Yu-WeiChen Gui-LaiYin LiShi Yan-LongXu Li-LiBi JingwangWang Qiang