The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
70 - 90% by HPLC.
- First try to dissolve a small amount of peptide in either water or buffer. The more charged residues on a peptide, the more soluble it is in aqueous solutions. - If the peptide doesn’t dissolve try an organic solvent e.g. DMSO, then dilute using water or buffer. - Consider that any solvent used must be compatible with your assay. If a peptide does not dissolve and you need to recover it, lyophilise to remove the solvent. - Gentle warming and sonication can effectively aid peptide solubilisation. If the solution is cloudy or has gelled the peptide may be in suspension rather than solubilised. - Peptides containing cysteine are easily oxidised, so should be prepared in solution just prior to use.
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Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
Information available upon request.
Lecithin cholesterol acyltransferase
Phosphatidylcholine sterol acyltransferase
Phospholipid cholesterol acyltransferase
Central enzyme in the extracellular metabolism of plasma lipoproteins. Synthesized mainly in the liver and secreted into plasma where it converts cholesterol and phosphatidylcholines (lecithins) to cholesteryl esters and lysophosphatidylcholines on the surface of high and low density lipoproteins (HDLs and LDLs). The cholesterol ester is then transported back to the liver. Has a preference for plasma 16:0-18:2 or 18:O-18:2 phosphatidylcholines. Also produced in the brain by primary astrocytes, and esterifies free cholesterol on nascent APOE-containing lipoproteins secreted from glia and influences cerebral spinal fluid (CSF) APOE- and APOA1 levels. Together with APOE and the cholesterol transporter ABCA1, plays a key role in the maturation of glial-derived, nascent lipoproteins. Required for remodeling high-density lipoprotein particles into their spherical forms.
Expressed mainly in brain, liver and testes. Secreted into plasma and cerebral spinal fluid. In liver, expressed in HEPG2 hepatocytes.
Defects in LCAT are the cause of lecithin-cholesterol acyltransferase deficiency (LCATD) [MIM:245900]; also called Norum disease. LCATD is a disorder of lipoprotein metabolism characterized by inadequate esterification of plasmatic cholesterol. Two clinical forms are recognized: familial LCAT deficiency and fish-eye disease. Familial LCAT deficiency is associated with a complete absence of alpha and beta LCAT activities and results in esterification anomalies involving both HDL (alpha-LCAT activity) and LDL (beta-LCAT activity). It causes a typical triad of diffuse corneal opacities, target cell hemolytic anemia, and proteinuria with renal failure. Defects in LCAT are a cause of fish-eye disease (FED) [MIM:136120]; also known as dyslipoproteinemic corneal dystrophy or alpha-LCAT deficiency. FED is due to a partial LCAT deficiency that affects only alpha-LCAT activity. It is characterized by low plasma HDL and corneal opacities due to accumulation of cholesterol deposits in the cornea ('fish-eye').
Belongs to the AB hydrolase superfamily. Lipase family.
O- and N-glycosylated. O-glycosylation on Thr-431 and Ser-433 consists of sialylated galactose beta 1-->3N-acetylgalactosamine structures. N-glycosylated sites contain sialylated triantennary and/or biantennary complex structures.
Secreted. Secreted into blood plasma. Produced in astrocytes and secreted into cerebral spinal fluid.