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Mouse Anti-LCAT Recombinant Antibody (CBYJL-1246) (CBMAB-L0781-YJ)

Provided herein is a Mouse monoclonal antibody, which binds to Lecithin-Cholesterol Acyltransferase (LCAT). The antibody can be used for immunoassay techniques, such as ELISA, IF, WB.
See all LCAT antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
CBYJL-1246
Antibody Isotype
IgG2a, κ
Application
ELISA, IF, WB

Basic Information

Immunogen
LCAT (AAH14781, 98 a.a. ~ 197 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa.Immunogen sequence: CWIDNTRVVY NRSSGLVSNA PGVQIRVPGF GKTYSVEYLD SSKLAGYLHT LVQNLVNNGY VRDETVRAAP YDWRLEPGQQ EEYYRKLAGL VEEMHAAYGK.
Specificity
Human
Antibody Isotype
IgG2a, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Buffer
PBS, pH 7.4
Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.
Epitope
aa 98-197

Target

Full Name
LCAT
Introduction
LCAT is the extracellular cholesterol esterifying enzyme, lecithin-cholesterol acyltransferase. The esterification of cholesterol is required for cholesterol transport. Mutations in this gene have been found to lead to fish-eye disease as well as LCAT deficiency. Among its related pathways are Lipoprotein metabolism and Metabolism.
Entrez Gene ID
UniProt ID
Function
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) (PubMed:10329423, PubMed:19065001, PubMed:26195816).
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 (PubMed:8820107).
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 (PubMed:10722751).
Catalyzes the hydrolysis of 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine (platelet-activating factor or PAF) to 1-O-alkyl-sn-glycero-3-phosphocholine (lyso-PAF) (PubMed:8016111).
Also catalyzes the transfer of the acetate group from PAF to 1-hexadecanoyl-sn-glycero-3-phosphocholine forming lyso-PAF (PubMed:8016111).
Catalyzes the esterification of (24S)-hydroxycholesterol (24(S)OH-C), also known as cerebrosterol to produce 24(S)OH-C monoesters (PubMed:24620755).
Biological Process
Cholesterol esterificationManual Assertion Based On ExperimentIDA:UniProtKB
Cholesterol homeostasisManual Assertion Based On ExperimentIDA:BHF-UCL
Cholesterol metabolic processManual Assertion Based On ExperimentIDA:UniProtKB
Cholesterol transportManual Assertion Based On ExperimentIDA:MGI
High-density lipoprotein particle remodelingManual Assertion Based On ExperimentIDA:UniProtKB
Lipid metabolic processManual Assertion Based On ExperimentIBA:GO_Central
Lipoprotein biosynthetic processIEA:Ensembl
Phosphatidylcholine biosynthetic processManual Assertion Based On ExperimentIDA:BHF-UCL
Phosphatidylcholine metabolic processManual Assertion Based On ExperimentIDA:UniProtKB
Phospholipid metabolic processManual Assertion Based On ExperimentIDA:BHF-UCL
Regulation of high-density lipoprotein particle assemblyIEA:Ensembl
Response to copper ionIEA:Ensembl
Response to glucocorticoidIEA:Ensembl
Reverse cholesterol transportManual Assertion Based On ExperimentIDA:BHF-UCL
Very-low-density lipoprotein particle remodelingManual Assertion Based On ExperimentIDA:BHF-UCL
Cellular Location
Secreted
Secreted into blood plasma (PubMed:3458198, PubMed:8820107, PubMed:10222237).
Produced in astrocytes and secreted into cerebral spinal fluid (CSF) (PubMed:10222237).
Involvement in disease
Lecithin-cholesterol acyltransferase deficiency (LCATD):
A disorder of lipoprotein metabolism characterized by inadequate esterification of plasmatic cholesterol. Two clinical forms are recognized: complete LCAT deficiency and fish-eye disease. LCATD is generally referred to the complete form which is associated with absence of both alpha and beta LCAT activities resulting 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.
Fish-eye disease (FED):
A disorder of lipoprotein metabolism due to partial lecithin-cholesterol acyltransferase deficiency that affects only alpha-LCAT activity. FED is characterized by low plasma HDL and corneal opacities due to accumulation of cholesterol deposits in the cornea ('fish-eye').
PTM
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.

Gao, H., Wu, J., Sun, Z., Zhang, F., Shi, T., Lu, K., ... & Xue, B. (2022). Influence of lecithin cholesterol acyltransferase alteration during different pathophysiologic conditions: A 45 years bibliometrics analysis. Frontiers in Pharmacology, 13, 1062249.

Vitali, C., Bajaj, A., Nguyen, C., Schnall, J., Chen, J., Stylianou, K., ... & Cuchel, M. (2022). A systematic review of the natural history and biomarkers of primary lecithin: cholesterol acyltransferase deficiency. Journal of lipid research, 63(3).

Sasaki, M., Delawary, M., Sakurai, H., Kobayashi, H., Nakao, N., Tsuru, H., ... & Kubota, K. (2021). Novel LCAT (lecithin: cholesterol acyltransferase) activator DS-8190a prevents the progression of plaque accumulation in atherosclerosis models. Arteriosclerosis, Thrombosis, and Vascular Biology, 41(1), 360-376.

Baragetti, A., Ossoli, A., Strazzella, A., Simonelli, S., Baragetti, I., Grigore, L., ... & Calabresi, L. (2020). Low plasma lecithin: cholesterol acyltransferase (LCAT) concentration predicts chronic kidney disease. Journal of Clinical Medicine, 9(7), 2289.

Norum, K. R., Remaley, A. T., Miettinen, H. E., Strøm, E. H., Balbo, B. E., Sampaio, C. A., ... & Retterstøl, K. (2020). Lecithin: cholesterol acyltransferase: symposium on 50 years of biomedical research from its discovery to latest findings. Journal of Lipid Research, 61(8), 1142-1149.

Ossoli, A., Simonelli, S., Varrenti, M., Morici, N., Oliva, F., Stucchi, M., ... & Calabresi, L. (2019). Recombinant LCAT (lecithin: cholesterol acyltransferase) rescues defective HDL (high-density lipoprotein)-mediated endothelial protection in acute coronary syndrome. Arteriosclerosis, thrombosis, and vascular biology, 39(5), 915-924.

Manthei, K. A., Yang, S. M., Baljinnyam, B., Chang, L., Glukhova, A., Yuan, W., ... & Tesmer, J. J. (2018). Molecular basis for activation of lecithin: cholesterol acyltransferase by a compound that increases HDL cholesterol. Elife, 7, e41604.

Yokoyama, K., Tani, S., Matsuo, R., & Matsumoto, N. (2018). Association of lecithin-cholesterol acyltransferase activity and low-density lipoprotein heterogeneity with atherosclerotic cardiovascular disease risk: a longitudinal pilot study. BMC Cardiovascular Disorders, 18(1), 1-10.

Gebhard, C., Rhainds, D., He, G., Rodés-Cabau, J., Lavi, S., Spence, J. D., ... & Tardif, J. C. (2018). Elevated level of lecithin: cholesterol acyltransferase (LCAT) is associated with reduced coronary atheroma burden. Atherosclerosis, 276, 131-139.

Oldoni, F., Baldassarre, D., Castelnuovo, S., Ossoli, A., Amato, M., van Capelleveen, J., ... & Calabresi, L. (2018). Complete and partial lecithin: cholesterol acyltransferase deficiency is differentially associated with atherosclerosis. Circulation, 138(10), 1000-1007.

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For research use only. Not intended for any clinical use.

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