Sandwich ELISA, Biotin-labelled antibody
Serum, Plasma-EDTA, Plasma-Heparin, Plasma-Citrate
Store the complete kit at 2–8°C. Under this condition, the kit is stable until the expiration date (see the label on the box).
Limit of Detection
n = 8; CV = 3.7%
n = 6; CV = 8.9%
- bovine Non-detectable
- cat Non-detectable
- dog Non-detectable
- goat Non-detectable
- hamster Non-detectable
- horse Non-detectable
- mouse Non-detectable
- pig Non-detectable
- rabbit Non-detectable
- rat Non-detectable
- sheep Non-detectable
- chicken Not tested
- human Yes
- monkey Yes (recommended dilution 1:3)
- It is intended for research use only
- The total assay time is less than 3.5 hours.
- The kit measures Angptl3 in serum and plasma (EDTA, citrate, heparin).
- Assay format - 96 wells
- Quality controls are human serum based. No animal sera are used.
- Standard is recombinant protein based.
- Components of kit are provided ready to use, concentrated or lyophilized.
Energy metabolism and body weight regulation, Oncology
Angiopoietin-like Protein 3 (Angptl3) is one from six members of Angiopoietin-like (Angptl) family of proteins, which has been identified as orphan ligands with structural similarity to angiopoietins. Angptl3 has 490-amino acid residues and its expression is restricted to the liver.
Angptl3 and Angptl4 have been shown to regulate fat, lipid or glucose metabolic homeostasis. Angptl3 is a hepatocyte-derived circulating factor that affect lipid metabolism and is involved in regulating lipid storage and breakdown.
Overexpression of Angptl3 or intravenous injection of the purified protein in mice elicited an increase in circulating plasma lipid levels. Angptl3 decreases very low density lipoprotein (VLDL) triglyceride clearance by inhibiting lipoprotein lipase (LPL) activity, directly targeting adipose cells to activate lipolysis. This results in an increased release of free fatty acid (FFA) and glycerol from adipocytes. These observations indicate that Angptl3 might regulate lipid metabolism by inhibiting LPL and by stimulating lipolysis in adipocytes.
Recent findings suggest that elevated levels of Angptl3 in diabetic states might be involved in inducing hypertriglyceridemia and hyperfattyacidemia in diabetes and obesity. Hypertriglyceridemia causes triglyceride accumulation in peripheral tissues such as skeletal muscles to enhance insulin- and leptin- resistance, and in vessel walls to induce atherosclerosis. Hyperfattyacidemia also affects the regulation of insulin secretion.
Taken together, these findings suggest that abnormalities in the regulation of Angptl3 might be involved in the pathogenesis of metabolic syndrome.
Angptl3 also suggest a possible role in the regulation of proliferation of new vessel from preexisting capillaries; a process termed angiogenesis also plays a key role in the progression of solid tumor growth, diabetic retinopathies, psoriasis, inflammation, and rheumathoid arthritis.
Areas of investigation: Lipid metabolism, Angiogenesis, Atherosclerosis