Lecithin Cholesterol Acyltransferase (LCAT) Recombinant Protein | LCAT recombinant protein

Recombinant Lecithin Cholesterol Acyltransferase (LCAT)

Cat. Num. AAA2010059

• Gene Names: Lcat; AI046659; D8Wsu61e
• Applications: SDS-Page, Western Blot, ELISA, Immunoprecipitation
• Purity: > 95%
• Synonyms: Lecithin Cholesterol Acyltransferase (LCAT); Recombinant Lecithin Cholesterol Acyltransferase (LCAT); LCAT recombinant protein

• Host: E Coli
• Purity/Purification: > 95%
• Form/Format: Supplied as lyophilized form in PBS,pH7.4, containing 5% sucrose, 0.01% sarcosyl.
• Sequence: The target protein is fused with N-terminal His-Tag, its sequence is listed below.; MGHHHHHHSGSEF-I STPNFNYTVQ DFERFFTDLH FEEGWHMFLQ SRDLLERLPA PGVEVYCLYG VGRPTPHTYI YDHNFPYKDP VAALYEDGDD TVATRSTELC GQWQGRQSQP VHLLPMNETD HLNMVFSNKT LEHINAILLG AYRTPKSPAA SP
• Sequence Length: 438

• Applicable Applications for LCAT recombinant protein: SDS-PAGE, Western Blot (WB), ELISA (EIA), Immunoprecipitation (IP)
• Organism: Mus musculus (Mouse)
• Expression System: Prokaryotic expression
• Residues: Ile290~Pro432 (Accession # P16301) with N-terminal His-Tag
• Endotoxin Level: <1.0EU per 1ug (determined by the LAL method)
• Reconstitution: Reconstitute in sterile PBS, pH7.2-pH7.4.
• Preparation and Storage: Avoid repeated freeze/thaw cycles. Store at 2-8 degree C for one month. Aliquot and store at -80 degree C for 12 months.; Stability Test: The thermal stability is described by the loss rate of the targetprotein. The loss rate was determined by accelerated thermal degradation test,that is, incubate the protein at 37 degree C for 48h, and no obvious degradation andprecipitation were observed. (Referring from China Biological Products Standard,which was calculated by the Arrhenius equation.) The loss of this protein is lessthan 5% within the expiration date under appropriate storage condition.

Sequence Information

SDS-Page

NCBI and Uniprot Product Information

• NCBI GI #: 244791354
• NCBI GeneID: 16816
• NCBI Accession #: NP_032516.2
• NCBI GenBank Nucleotide #: NM_008490.2
• UniProt Accession #: P16301; Q8K139
• Molecular Weight: 17.9kDa
• NCBI Official Full Name: phosphatidylcholine-sterol acyltransferase
• NCBI Official Synonym Full Names: lecithin cholesterol acyltransferase
• NCBI Official Symbol: Lcat
• NCBI Official Synonym Symbols: AI046659; D8Wsu61e
• NCBI Protein Information: phosphatidylcholine-sterol acyltransferase; phospholipid-cholesterol acyltransferase; lecithin-cholesterol acyltransferase Lcat
• UniProt Protein Name: Phosphatidylcholine-sterol acyltransferase
• UniProt Gene Name: Lcat
• UniProt Entry Name: LCAT_MOUSE

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

Cellular Component: extracellular space; extracellular region

Molecular Function: apolipoprotein A-I binding; phospholipase A2 activity; transferase activity; transferase activity, transferring acyl groups; phosphatidylcholine-sterol O-acyltransferase activity; O-acyltransferase activity

Biological Process: steroid metabolic process; cholesterol metabolic process; cholesterol homeostasis; cholesterol transport; reverse cholesterol transport; response to copper ion; lipoprotein biosynthetic process; phospholipid metabolic process; response to glucocorticoid stimulus; phosphatidylcholine biosynthetic process; lipoprotein metabolic process; lipid metabolic process