Rabbit anti-Human LCAT Polyclonal Antibody | anti-LCAT antibody

Anti-LCAT Antibody, Rabbit Polyclonal

Cat. Num. AAA8106879

• Reactivity: Human
• Applications: ELISA, Immunohistochemistry
• Purity: Protein A & Antigen Affinity
• Synonyms: LCAT; Polyclonal Antibody; Anti-LCAT Antibody; Rabbit Polyclonal; LCAT Antibody; Rabbit PAb; Antigen Affinity Purified; lecithin-cholesterol acyltransferase; anti-LCAT antibody

• Host: Rabbit
• Reactivity: Human
• Clonality: Polyclonal
• Isotype: Rabbit IgG
• Specificity: Human LCAT
• Purity/Purification: Protein A & Antigen Affinity
• Form/Format: Liquid; 0.2um filtered solution in PBS

• Applicable Applications for anti-LCAT antibody: ELISA (EIA), Immunohistochemistry-Paraffin (IHC-P)
• Application Notes: ELISA: 1:5000-1:10,000; IHC-P: 1:500-1:2000
• Immunogen: Recombinant Human LCAT Protein
• Conjugation: Unconjugated
• Preparation: Produced in rabbits immunized with purified, recombinant Human LCAT (rh LCAT). LCAT specific IgG was purified by Human LCAT affinity chromatography.
• Preparation and Storage: This antibody can be stored at 2-8 degree C for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20 degree C to -80 degree C. Preservative-Free. Avoid repeated freeze-thaw cycles.

Immunohistochemistry (IHC)

(Immunochemical staining of human LCAT in human liver with rabbit polyclonal antibody at 1:1000 dilution, formalin-fixed paraffin embedded sections.)

Related Product Information for anti-LCAT antibody

Lecithin: cholesterol acyltransferase (LCAT) is the sole enzyme that esterifies cholesterol in plasma, thus determining the maturation of high-density lipoproteins. Because it maintains an unesterified cholesterol gradient between peripheral cells and extracellular acceptors, for a long time, LCAT has been considered as a key enzyme in reverse cholesterol transport. Lecithin cholesterol acyltransferase (LCAT) plays a pivotal role in HDL metabolism.LCAT is intimately involved in HDL maturation and is a key component of the reverse cholesterol transport (RCT) pathway which removes excess cholesterol molecules from the peripheral tissues to the liver for excretion. LCAT may also modify oxidative and inflammatory processes, as supported by an inverse relationship with HDL antioxidative functionality and a positive relationship with high-sensitivity C-reactive protein (hsCRP).

NCBI and Uniprot Product Information

• NCBI GI #: 4557892
• NCBI GeneID: 3931
• NCBI Accession #: NP_000220.1
• NCBI GenBank Nucleotide #: NM_000229.1
• UniProt Accession #: P04180; Q53XQ3
• NCBI Official Full Name: phosphatidylcholine-sterol acyltransferase
• NCBI Official Synonym Full Names: lecithin-cholesterol acyltransferase
• NCBI Official Symbol: LCAT
• NCBI Protein Information: phosphatidylcholine-sterol acyltransferase; phospholipid-cholesterol acyltransferase
• UniProt Protein Name: Phosphatidylcholine-sterol acyltransferase
• UniProt Gene Name: LCAT
• UniProt Entry Name: LCAT_HUMAN

Uniprot Description

LCAT: 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. Defects in LCAT are the cause of lecithin-cholesterol acyltransferase deficiency (LCATD); 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); 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.

Protein type: Secreted, signal peptide; Secreted; Lipid Metabolism - glycerophospholipid; EC 2.3.1.43; Transferase

Chromosomal Location of Human Ortholog: 16q22.1

Cellular Component: extracellular space; extracellular region

Molecular Function: apolipoprotein A-I binding; protein binding; phosphatidylcholine-sterol O-acyltransferase activity

Biological Process: cholesterol metabolic process; cholesterol homeostasis; reverse cholesterol transport; cholesterol transport; lipoprotein biosynthetic process; phospholipid metabolic process; phosphatidylcholine biosynthetic process; lipoprotein metabolic process

Disease: Lecithin:cholesterol Acyltransferase Deficiency; Fish-eye Disease