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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- Hypertriglyceridemia is associated with increased atherosclerotic cardiovascular disease and pancreatitis risk, yet durable triglyceride reduction remains challenging. Olezarsen, an antisense oligonucleotide targeting APOC3, substantially reduced triglycerides in phase 3 trials. Fibrates lower triglycerides through complementary lipoprotein lipase and apolipoprotein C-III (APOC3) pathways. Whether fibrate therapy modifies olezarsen's effects is unknown. - Source: PubMed
Publication date: 2026/08/12
Wang Annabel ZAlexander Veronica JProhaska Thomas ARan XinhuiGoodrich Erica LMurphy Sabina AZimerman AndréMoura Filipe AKang Yu MiNordestgaard Børge GStroes Erik S GGaudet DanielBadimon LinaDuarte Joao SequeiraFerreira JorgeVinereanu DragosPella DanielDzupina AndrejTsimikas SotiriosGiugliano Robert PSabatine Marc SMarston Nicholas ABergmark Brian A - FOXO6 is a member of the FOXO transcription factor family that differs from FOXO1, FOXO3, and FOXO4 in its nucleocytoplasmic regulation, remaining predominantly within the nucleus because it lacks a functional nuclear export sequence. FOXO6 activity can nevertheless be inhibited by insulin/AKT signaling, whereas impaired insulin signaling increases its transcriptional activity in hepatocytes under insulin-resistant and nutrient-rich conditions. Recent studies indicate that FOXO6 regulates hepatic metabolic pathways associated with oxidative injury, inflammatory signaling, and lipid accumulation. In hepatocellular carcinoma, increased FOXO6 expression is associated with glycolytic activity, proliferation, and invasion. We recently reported that FOXO6-dependent transcriptional regulation contributes to reactive oxygen species (ROS) production and inflammasome-associated inflammatory signaling through induction of thioredoxin-interacting protein (TXNIP). Furthermore, FOXO6 regulates lipid metabolic pathways through transcriptional activation of apolipoprotein C3 (ApoC3) and peroxisome proliferator-activated receptor (PPAR) γ together with suppression of PPARα, thereby promoting triglyceride accumulation, mitochondrial dysfunction, and lipotoxic injury in hepatocytes. These metabolic and inflammatory alterations contribute to hepatic steatosis, mitochondrial injury, and inflammatory hepatocellular damage. In hepatocellular carcinoma, increased FOXO6 expression is associated with glycolytic metabolism, angiogenic signaling, proliferative activity, immune suppression, and invasive phenotypes. FOXO6-dependent signaling interacts with STAT3, NF-κB, and β-catenin pathways involved in metabolic adaptation and tumor progression. Recent studies demonstrate relationships between increased FOXO6 expression, vascular invasion, aggressive tumor phenotypes, and reduced survival in hepatocellular carcinoma. This review examines FOXO6-associated transcriptional mechanisms involved in hepatic metabolic inflammation and hepatocarcinogenesis. - Source: PubMed
Kim Mi EunKim YukyeongLee Jun Sik - Apolipoprotein C-III (apoC-III) regulates triglyceride-rich lipoprotein metabolism. ION775 is a GalNAc-conjugated small interfering RNA designed to silence APOC3 mRNA and enable infrequent dosing. - Source: PubMed
Publication date: 2026/08/28
Tsimikas SotiriosMorgan ErinSharma JyotiLin TaoMullick Adam EPrakash Thazha PSwayze Eric EProhaska Thomas A - Prediabetes associates with increased production of triglyceride-rich lipoproteins (TRLs), cardiovascular disease (CVD), and hepatic steatosis, which is linked to increased plasma levels of soluble TREM2 (sTREM2), the shed domain of TREM2 (triggering receptor expressed on myeloid cells 2). Whether and how TREM2 shedding contributes to elevated TRLs is unknown. By complementary analyses of individuals with prediabetes and hepatic steatosis and preclinical models, we show that plasma sTREM2 levels correlate positively with plasma apolipoprotein C3 (APOC3), an apolipoprotein that slows TRL catabolism and predicts CVD risk. Individuals with prediabetes and hepatic steatosis had higher plasma concentrations of APOC3-rich TRLs 35 to 60 nm in diameter than healthy controls. Mouse models of prediabetes with hepatic steatosis revealed that the increased plasma concentrations of sTREM2, APOC3, and TRLs were due to activation of macrophage ADAM17, a TREM2 sheddase. Preserving macrophage full-length TREM2 protected against the elevated plasma APOC3, sTREM2, dyslipidemia, and atherosclerosis, while TREM2-deficiency increased APOC3, TRLs, and atherosclerosis. Mechanistically, full-length TREM2 mediates macrophage TRL uptake, preventing excessive hepatic APOC3-rich TRL release and atherosclerosis. Our findings identify macrophage TREM2 shedding as an upstream contributor to the elevated TRLs in hepatic steatosis, providing a mechanistic link between hepatic steatosis and CVD risk in prediabetes. - Source: PubMed
Publication date: 2026/08/27
Tang JingjingKanter JennyShao BaohaiShimizu-Albergine MasamiKramer FarahKhang Ah ReumLuo JasonZheng HuaqingTran AlanCervantes JocelynFrey Jeremy MDorfman Mauricio DHsu Cheng-Chiehden Hartigh Laura JVaisar TomasDavies Brandon SjMullick Adam EIoannou GeorgeSmith Gordon IKlein SamuelDavidson Nicholas OBornfeldt Karin E - Genetic clusters related to Type 2 diabetes (T2D) have differential impact on cardiovascular diseases (CVDs), although the underlying mechanisms, such as proteomic perturbation, remain unexplored. We conducted a network Mendelian randomisation (MR) study to identify proteomic mediators linking T2D genetic clusters and CVDs. - Source: PubMed
Publication date: 2026/08/24
Liao ShuangSung Gabriel Chun YinLiang YiwenLi ChenxiAu Yeung Shiu Lun