|CSC-DC000785||Panoply™ Human APOC3 Knockdown Stable Cell Line||Inquiry|
|CSC-SC000785||Panoply™ Human APOC3 Over-expressing Stable Cell Line||Inquiry|
|CDCB166032||Chicken APOC3 ORF Clone (NM_001302127)||Inquiry|
|CDCB191944||Rabbit APOC3 ORF clone (XM_002708371.2)||Inquiry|
|CDCR277747||Human APOC3 ORF Clone(NM_000040.1)||Inquiry|
|CDCR377410||Rat Apoc3 ORF Clone(NM_012501.2)||Inquiry|
|CDCS405370||Human APOC3 ORF Clone (BC027977)||Inquiry|
|CDCS405371||Human APOC3 ORF Clone (BC121081)||Inquiry|
|CDFH000986||Human APOC3 cDNA Clone(NM_000040.1)||Inquiry|
|MiUTR1H-00478||APOC3 miRNA 3'UTR clone||Inquiry|
|MiUTR1M-01586||APOC3 miRNA 3'UTR clone||Inquiry|
|SHG065707||shRNA set against Mouse Apoc3(NM_023114.3)||Inquiry|
|SHG065743||shRNA set against Human APOC3(NM_000040.1)||Inquiry|
|SHH238506||shRNA set against Human APOC3 (NM_000040.1)||Inquiry|
|SHH238510||shRNA set against Mouse APOC3 (NM_023114.3)||Inquiry|
|SHH238514||shRNA set against Rat APOC3 (NM_012501.2)||Inquiry|
|SHW004557||shRNA set against Chicken APOC3 (NM_001302127)||Inquiry|
Apolipoprotein C3 (APOC3) is high in C family and mainly regulates the decomposition and metabolism of triglyceride-rich lipoproteins (TRLs). APOC3 is a special highlight in the field of lipoprotein and arteriosclerosis research in recent years. A large number of studies have shown that APOC3 is involved in lipid metabolism and is a risk factor for cardiovascular disease.
Apolipoprotein C is a water-soluble low molecular weight protein mainly distributed in the surface of plasma high density lipoprotein (HDL), very low density lipoprotein (VLDL) and chylomicron (CM). The β-O-glycosidic bond of APOC3 can be linked to the hydroxyl group of the 74th threonine residue on the peptide chain to form a single-chain polypeptide. According to the number of sialic acid residues in the 74th threonine residue of APOC3, it can be divided into three subtypes: APOC30, APOC31 and APOC32. Among them, APOC31 and APOC32 are the main forms of APOC3. During LPL hydrolysis of VLDL, APOC3 is transferred from VLDL to HDL and then back to the nascent VLDL surface. Studies have shown that APOC3 can be quickly exchanged between TRLs and HDL. It is suggested that APOC3 is in a dynamic balance in the body.
APOC3 and Plasma Triglyceride Metabolism
Studies by Daniel et al. showed that when plasma triglyceride (TG) levels were normal (<150 mg/dl [1.7 mmol per liter]), there was considerable ability to absorb triglycerides. Triglycerides come from two sources: the liver (in the form of very low density lipoprotein (VLDL)) and dietary fat (in the form of chylomicrons) through the intestine. Triglyceride production occurs primarily through a lipoprotein lipase (LPL)-dependent pathway, and to a lesser extent through the LPL-independent pathway, and the study of this pathway is not well understood. APOC3 regulates TG metabolism by inhibiting an LPL-dependent pathway or one or more LPL-independent pathways.
Figure 1. Plasma Triglyceride Metabolism and the Role of APOC3. (Daniel,.et al.2014)
APOC3 and Cardiovascular Disease
The level of APOC3 in plasma is increased, the concentration of TG is increased, insulin resistance is aggravated, and cardiovascular disease and type 2 diabetes are induced. APOC3 is positively correlated with TG levels and is a risk factor for cardiovascular disease. Animal-level studies support a positive correlation between APOC3 levels and cardiovascular disease incidence. In APOC3 transgenic mice, the concentration of APOC3 in the blood increased, and the level of TG increased, which accelerated the development of atherosclerosis. In APOC3 knockout mice, TG levels were significantly reduced, which protected cardiovascular function. The investigators found that a large sample of long-term follow-up studies found that patients with myocardial infarction had significantly higher levels of APOC3 in plasma LDL than those without myocardial infarction. This suggests that the more APOC3 proteins in LDL, the greater the risk of cardiovascular disease. LDL can be considered a high-risk factor for cardiovascular disease to a certain extent because LDL contains APOC3 protein.
A joint study of the genome confirmed that the genes on the ApoAⅠ/CⅢ /AⅣ gene cluster play a role in maintaining TG levels and have a certain effect on the occurrence of cardiovascular disease. Crosby et al. showed that there are many variations in the human APOC3 gene, including three loss-of-function mutations: nonsense mutation (R19X) and two splice site mutations (IVS2 + 1G→A and IVS3 + 1G→T) and one Missense mutation (A43T). Among them, the main mutation is R19X. The APOC3 gene nonsense mutation R19X, that is, the cytosine at the 55th base from the translation initiation site was replaced by thymine, resulting in the 19th arginine becoming the stop codon. The level of plasma APOC3 protein in R19X mutant carriers was lower than that in normal subjects, and the concentrations of fasting TG and VLDL were significantly decreased.
Crosby et al. independently verified that APOC3 functional mutations have a protective effect on cardiovascular disease. Jã ̧Rgensen et al. have shown that plasma APOC3 protein levels are positively correlated with the incidence of coronary heart disease. Epidemiology confirmed the APOC3 gene mutation, and the risk of ischemic cardiovascular disease and coronary heart disease decreased significantly. APOC3 gene polymorphism is closely related to cardiovascular disease. C3238 gene mutation increases TG and APOC3 levels, T-455C mutation down-regulates APOC3 gene expression, and the probability of cardiovascular disease is significantly reduced.
Saleheen et al. studied the lipid metabolism characteristics of human homozygous ApoC3 deficiency family and proposed a new theory of human gene knockout. They found that the APOC3 gene was missing from a population of dozens of small Pakistani fishing villages where marriages were commonplace. In a 28-person family, one man had a double-copy of the APOC3 gene missing, and his wife (and his cousin) was also missing. Their 9 children also lack the APOC3 gene. The levels of triglycerides in these naturally deleted populations are very low. Compared to normal family members, these people did not increase plasma triglyceride levels after a high-fat diet. This finding explains why a high-fat diet does not cause heart disease due to a functional deletion mutation in APOC3. According to Saleheen, "These are the first in the world to identify APOC3 knockouts in humans. Their genetic makeup provides a unique new understanding of the biological function of APOC3, which may further help confirm that inhibition of APOC3 is a treatment target for cardiac metabolic diseases." All of the above indicate that there is a causal relationship between APOC3 levels and cardiovascular disease risk.
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