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anti-Human APOC3 Antibodies:
anti-Mouse (Murine) APOC3 Antibodies:
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Human Polyclonal APOC3 Primary Antibody for ELISA, IHC - ABIN5596680
Takinami, Yoshimatsu, Uchiumi, Toyosaki-Maeda, Morita, Ishihara, Yamane, Fukuda, Okamoto, Numata, Fukui: Identification of potential prognostic markers for knee osteoarthritis by serum proteomic analysis. in Biomarker insights 2013
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Human Polyclonal APOC3 Primary Antibody for IHC (p), IP - ABIN153496
Wang, Song, Wagner, Pachuk, Subramanian: Development of a sensitive ELISA to quantify apolipoprotein CIII in nonhuman primate serum. in Journal of lipid research 2011
Show all 2 Pubmed References
Human Polyclonal APOC3 Primary Antibody for ELISA, WB - ABIN542606
Valleix, Verona, Jourde-Chiche, Nédelec, Mangione, Bridoux, Mangé, Dogan, Goujon, Lhomme, Dauteuille, Chabert, Porcari, Waudby, Relini, Talmud, Kovrov, Olivecrona, Stoppini, Christodoulou, Hawkins et al.: D25V apolipoprotein C-III variant causes dominant hereditary systemic amyloidosis and confers cardiovascular protective lipoprotein profile. ... in Nature communications 2016
High density lipoprotein with apolipoprotein C-III is associated with carotid intima-media thickness among generally healthy individuals.
there is a strong association between ApoC-III and FVIIa-AT levels in coronary artery disease
Our results suggest that genotype effects in APOC3 on hypertension risk have been shown in lean carriers of the C allele of C1100T and in less active people having the C allele of T-455C and T allele of C-482T in a large sample of the Korean population.
Meta-analysis: The low risk of ischemic vascular disease observed in APOC3 loss-of-function heterozygotes is mainly mediated by the associated low remnant cholesterol and not by low LDL-C.
ApoCIII may mediate the effects of ANGPTL8 on triglyceride metabolism.
The S2 allele of the SstI polymorphism in the apoC3 gene is associated with plasma apoCIII levels in the Li population. In combination with unfavorable lipid profiles, this might contribute to susceptibility to atherosclerosis.
Data indicate effects of a loss-of-function Ala43Thr substitution in apolipoprotein C3 (APOC3) rs147210663.
the present study demonstrates major modifications of the proteome in patients with cerebral lacunar infarction(LACI). The ApoC-III enrichment of the HDL of patients with cerebral lacunar infarction may cause a reduction in the anti-inflammatory ability of HDL, which may contribute to the progression of the disease
rs670, rs2854116, and rs662799 single nucleotide polymorphisms of the APOA1-C3-A5 cluster are associated with ischemic stroke in the northern Chinese Han population.
C3(QK) variant is a gain-of-function mutation that can stimulate VLDL1 production, through enhanced DNL
Review/Meta-analysis: APOC3 polymorphisms were not association with increased risk of ischemic stroke
rs4225 in the 3'-UTR of APOC3 might contribute to the risk of coronary heart disease by interfering with miR-4271 binding.
APOC3 modulates HDL structure and function, while it selectively promotes BAT metabolic activation
apoC-III potently inhibits triglyceride hydrolysis when LPL is bound to GPIHBP1
apolipoprotein C3 and atherosclerosis
intestinal apoC-III overexpression results in the secretion of smaller, less dense chylomicron particles along with reduced triacylglycerol secretion from the intestine
Aromatic residues in the C terminus of apolipoprotein C-III mediate lipid binding and LPL inhibition
No evidence that APOC3 3'UTR variant SstI modulates expression of liver/intestinal miRNAs in hypertriglyceridemia.
A rare variant in APOC3(rs138326449) has been associated with triglyceride, very low-density lipoprotein, and high-density lipoprotein levels, as well as risk of coronary heart disease. Effects are unlikely to be solely predictable by the action of APOC3 through LPL.
both human APOC3 A43T heterozygotes and mice expressing human APOC3 A43T display markedly reduced circulating apoC-III levels. In mice, this reduction is due to impaired binding of A43T apoC-III to lipoproteins and accelerated renal catabolism of free apoC-III.
Both triglyceride-rich lipoproteins (TRLs) and ApoCIII contribute to the progression of atherosclerosis, and the modulation of TRLs and ApoCIII may represent a novel therapeutic approach against hypertriglyceridemia induced atherosclerosis.
ApoC-III inhibits turnover of TG-rich lipoproteins primarily through a hepatic clearance mechanism mediated by the LDLR/LRP1 axis
These data strongly suggest that intestinal apoC-III is not a FoxO1 target and support the idea that apoC-III is not regulated coordinately with hepatic apoC-III, and establishes another key aspect of apoC-III that is unique in the intestine from the liver.
APOC3, whose dysregulation is liable for hypertriglyceridemia, is not a predisposing factor for linking overnutrition to NAFLD in obesity
Severe hypertriglyceridaemia resulting from ApoCIII overexpression promotes restenosis and atherosclerosis
Under conditions of islet insulin resistance, locally produced apoCIII is an important diabetogenic factor involved in impairment of beta-cell function.
decreased ApoAI synthesis might be accounted for the lower plasma HDL level in ApoCIII transgenic mice
ApoCIII hyperactivates beta cell CaV1 channels through SR-BI/beta1 integrin-dependent coactivation of PKA and Src.
Increased plasma APOC3 concentrations predispose mice to diet-induced nonalcoholic fatty liver and hepatic insulin resistance.
Glucose induces apoCIII transcription, which may represent a mechanism linking hyperglycemia, hypertriglyceridemia, and cardiovascular disease in type 2 diabetes.
PGC-1beta regulates plasma triglyceride metabolism through stimulating apolipoprotein C3 (APOC3) expression and elevating APOC3 levels in circulation
The apoC-III metabolism may contribute to dyslipidemia in CKD, and this requires further investigation.
Association between SstI polymorphism of the gene, glucose intolerance and cardiovascular risk in renal transplant recipients
ApoB lipoproteins that contain apoCIII increase THP-1 cell adhesion to ECs via PKCalpha and RhoA-mediated beta1-integrin activation.
oxidized fatty acids may act through an APOA5/APOClll mechanism that contributes to lowering of TG levels other than PPAR* induction
the apoCIII enhancer contributes to the maintenance of an active chromatin subdomain of the apoAI/CIII/AIV genes, but not apoAV
These results suggest that apoC-III may play a specific role in lipid storage and mobilization in adipocytes, non-lipoprotein-secreting cells, and indicate the functional role of RXRalpha during adipocyte differentiation.
gene polymorphisms in APOA5 and APOC3 are associated with meat quality traits in Kele pigs
changes in apolipoprotein A-I and apo C-III mRNA were reflected in their corresponding plasma levels
apoC-I and apoC-III inhibit lipolysis by displacing LPL from lipid emulsion particles. We also propose a role for these apolipoproteins in the irreversible inactivation of LPL by factors such as angptl4.
Apolipoprotein C-III is a very low density lipoprotein (VLDL) protein. APOC3 inhibits lipoprotein lipase and hepatic lipase\; it is thought to delay catabolism of triglyceride-rich particles. The APOA1, APOC3 and APOA4 genes are closely linked in both rat and human genomes. The A-I and A-IV genes are transcribed from the same strand, while the A-1 and C-III genes are convergently transcribed. An increase in apoC-III levels induces the development of hypertriglyceridemia.
, apolipoprotein C3
, apolipoprotein C-3
, apolipoprotein CIII