Polyclonal Rabbit APOA5 Antibody
- Known as:
- Polyclonal Rabbit APOA5 Antibody
- Catalog number:
- KA0246
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit APOA5 Antibody
Related genes to: Polyclonal Rabbit APOA5 Antibody
- 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: Polyclonal Rabbit APOA5 Antibody
Related articles to: Polyclonal Rabbit APOA5 Antibody
- 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 - Genome-wide association studies have identified >100 loci associated with metabolic dysfunction-associated steatotic liver disease (MASLD), yet the mechanisms by which noncoding variants alter disease risk remain unclear. Here we map chromatin accessibility in human MASLD liver nuclei, revealing enrichment of risk variants within cell-type-specific regulatory elements bound by lineage-determining transcription factors. Using a massively parallel reporter assay, we identified hundreds of differential activity variants (DAVs) that act in a cell-type-dependent and stimulus-dependent manner and perturb transcriptional regulatory networks linked to liver pathology. Integration of liver expression quantitative trait loci, chromatin looping and single-cell CRISPR interference screening assigns target genes to these DAVs. Importantly, DAVs at numerous loci, including SLC22A3 and key triglyceride metabolism regulators (APOA5, ANGPTL3 and LPL), modulate gene expression, lipid metabolism and hepatic stellate cell activation. Moreover, these DAVs allow improved prediction of MASLD risk. These results define a regulatory framework linking noncoding genetic variation to MASLD pathogenesis. - Source: PubMed
Publication date: 2026/06/02
Zhu BiyingHe NaXiao YangChen BinLi ChenMandla RaviLiu YifanZhang JiayuChang XiaoYu FulongVujkovic MarijanaLynch Julie AChang Kyong-Mi Pasaniuc BogdanRader Daniel JLazar Mitchell AHu Wenxiang - Hypertriglyceridemia arises from complex interactions between genetic and dietary factors. AMY1A/AMY2B copy number variation (CNV) and APOA5 rs651821 have been associated with triglyceride metabolism, and their effects may be modified by carbohydrate intake. This study investigated the combined influence of AMY1A/AMY2B CNV, APOA5 rs651821, and dietary carbohydrate intake on the odds of hypertriglyceridemia in middle-aged Korean adults. - Source: PubMed
Publication date: 2026/05/19
Kim MinyeongKo Seong-HeeKim SubinShin Dayeon - Mutations of LDLR, APOB and PCSK9 have been well-established to cause hypercholesterolemia while the pathogenic effects of LPL has been confirmed by cohorts and functional studies in hypertriglyceridemia. However, these mutations do not fully account for all dyslipidemia, and it remains unexplained why some patients with dyslipidemia develop coronary heart disease (CHD) while others do not. - Source: PubMed
Publication date: 2026/05/12
Huang ManSong XiuliZhou ShuniZhang HaiyanHe LijuanChen YanghuiChen GuangzhiDing HuJiang JiangangWang YanWang Dao WenSun YangWang Hong - Familial chylomicronemia syndrome (FCS) is a severe, life-threatening genetic disorder resulting from pathogenic variants in genes involved in lipoprotein lipase (LPL) function, including LPL, APOC2, APOA5, GPIHBP1, and LMF1. - Source: PubMed
Publication date: 2026/04/02
Aboheimed Ghada IAlRasheed Maha MAlfattani Areej AAlhusayn Khalid OAlali Shog MAlkhbiah Reema AColak DilekAlashwal AbdullahKaya Namik