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), characterized by a cluster of interrelated metabolic abnormalities including central obesity, elevated blood pressure, dysglycemia, hypertriglyceridemia, and reduced high-density lipoprotein cholesterol (HDL-C), substantially increases type 2 diabetes and cardiovascular disease risk. Conventional genome-wide association studies (GWASs) analyze individual traits or a dichotomized MetS status, only partially capturing its heritability and potentially overlooking variants with shared (pleiotropic) effects across correlated traits. Here, we performed a multiple-trait GWAS using data from the Korean Genome and Epidemiology Study. Using the Korea Biobank Array (K-Chip), we analyzed a discovery cohort from the Ansan and Ansung studies (1490 cases and 3856 controls) and validated the findings in CAVAS (3620 cases and 4461 controls) and HEXA (15,257 cases and 41,807 controls) cohorts. We jointly modeled six MetS-related traits using the complementary multivariate frameworks Multiple Phenotype Association Tests and Genome-wide Efficient Mixed Model Association, alongside a baseline logistic regression. Whereas logistic regression detected 2 variants (rs662799 and rs2075291), the multivariate analyses identified 79 significant single-nucleotide polymorphisms; all were replicated in the HEXA cohort. Functional annotation prioritized 27 high-risk variants mapping to 12 genes, whereas pathway analysis (DAVID) implicated eight Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathways related to lipid metabolism. Our findings demonstrate that multivariate analysis substantially improves the identification of pleiotropic susceptibility loci for MetS in the Korean population and indicates candidate genes for early detection and management. - Source: PubMed
Publication date: 2026/09/09
Kim DasomCha JunhoChoi Sungkyoung - 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