Abcam, ab175019, Anti-LCAT antibody [EPR1383(2)] - BSA and Azide free

Size: 100µg / 1mg
Rabbit Recombinant Monoclonal LCAT antibody. Carrier free. Suitable for IHC-P, WB and reacts with Human samples. Cited in 1 publication.
Key facts
Host species:Rabbit,
Clonality:Monoclonal,
Clone number:EPR1383(2),
Isotype:IgG,
Carrier free:Yes,
Reacts with:Human,
Applications:IHC-P, WBSee reactivity dataSee the reactivity data table below for information on validated species and application combinations.,
Immunogen:The exact immunogen used to generate this antibody is proprietary information.

Product details:
ab175019 is the carrier-free version of
ab109417
Patented technology
Our RabMAb
technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to
RabMAb® patents
What are the advantages of a recombinant monoclonal antibody?
This product is a recombinant monoclonal antibody, which offers several advantages including:
- High batch-to-batch consistency and reproducibility
- Improved sensitivity and specificity
- Long-term security of supply
- Animal-free batch production
For more information, read more on
recombinant antibodies
Conjugation ready
Our carrier-free antibodies are typically supplied in a PBS-only formulation, purified and free of BSA, sodium azide and glycerol. This conjugation-ready format is designed for use with fluorochromes, metal isotopes, oligonucleotides, and enzymes, which makes them ideal for antibody labelling, functional and cell-based assays, flow-based assays (e.g. mass cytometry) and Multiplex Imaging applications.
Use our
conjugation kits
for antibody conjugates that are ready-to-use in as little as 20 minutes with 1 minute hands-on-time and 100% antibody recovery: available for fluorescent dyes, HRP, biotin and gold.
Compatibility
This product is compatible with the Maxpar
Antibody Labeling Kit from Fluidigm, without the need for antibody preparation. Maxpar
is a trademark of Fluidigm Canada Inc.

Properties and Storage Information:
Form-Liquid, Purification technique-Affinity purification Protein A, Storage buffer-Constituents: PBS, Shipped at conditions-Blue Ice, Appropriate short-term storage conditions-+4°C, Appropriate long-term storage conditions-+4°C, Storage information-Do Not Freeze

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
LCAT also known as lecithin-cholesterol acyltransferase is an enzyme with a molecular mass of approximately 68 kDa. It belongs to the family of esterases and is mainly expressed in the liver. LCAT circulates in the bloodstream playing a significant role in lipid metabolism by catalyzing the formation of cholesteryl esters from free cholesterol and phosphatidylcholine (lecithin) on the surface of high-density lipoproteins (HDL).
Biological function summary
This enzyme functions centrally in the maturation of high-density lipoprotein particles. LCAT interacts with and acts upon HDL converting nascent HDL into mature HDL by catalyzing the esterification of cholesterol. This process results in the sequestration of cholesterol within the core of HDL particles essential for reverse cholesterol transport to the liver. Moreover LCAT does not operate as part of a larger complex but is an active enzyme on its own within various lipid transport processes.
Pathways
LCAT's action significantly influences the lipid metabolism and reverse cholesterol transport pathways. In the lipid metabolism pathway it works closely with apolipoproteins such as apoA-I which serves as an activator. ApoA-I stabilizes the enzymatic action of LCAT promoting cholesterol homeostasis whereas LCAT ensures the efficient transfer of cholesterol to the liver within the reverse cholesterol transport pathway contributing to the maintenance of lipid balance.
LCAT deficiency can lead to conditions like familial LCAT deficiency and Fish Eye disease. These disorders are marked by abnormal cholesterol and lipid accumulation due to impaired LCAT activity. Apolipoproteins particularly apoA-I also demonstrate a significant connection as mutations or lack of apoA-I compromise LCAT activation exacerbating hyperlipidemia and related lipid disorders.