Rabbit Anti-APOA1 Recombinant Antibody (BA0385) (CBMAB-0073CQ)

Rabbit

Human

BA0385

IgG

ELISA

Human Apolipoprotein A-I/APOA1.

Rabbit

Human

IgG

Monoclonal

The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Application	Note
ELISA	1:5,000-1:10,000

Liquid

PBS, pH 7.4

None

Batch dependent

>95% as determined by analysis by SDS-PAGE

Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Apolipoprotein A1

This gene encodes apolipoprotein A-I, which is the major protein component of high density lipoprotein (HDL) in plasma. ApoA-I is a cofactor for LCAT, which is responsible for the formation of most cholesteryl esters in plasma. ApoA-I also promotes efflux of cholesterol from cells. The liver and small intestine are the sites of synthesis of apoA-I. Defects in this gene are associated with HDL deficiencies, including Tangier disease, and with systemic non-neuropathic amyloidosis.

Apolipoprotein A-I; Apo-AI; Apolipoprotein A1; ApoA-I

Participates in the reverse transport of cholesterol from tissues to the liver for excretion by promoting cholesterol efflux from tissues and by acting as a cofactor for the lecithin cholesterol acyltransferase (LCAT). As part of the SPAP complex, activates spermatozoa motility.

Adrenal gland development Source: Ensembl
Amyloid fibril formation Source: Reactome
Animal organ regeneration Source: Ensembl
Blood vessel endothelial cell migration Source: Ensembl
Cellular protein metabolic process Source: Reactome
Cholesterol biosynthetic process Source: GO_Central
Cholesterol efflux Source: BHF-UCL
Cholesterol homeostasis Source: BHF-UCL
Cholesterol import Source: BHF-UCL
Cholesterol metabolic process Source: BHF-UCL
Cholesterol transport Source: MGI
Chylomicron assembly Source: Reactome
Chylomicron remodeling Source: Reactome
Endothelial cell proliferation Source: Ensembl
Glucocorticoid metabolic process Source: Ensembl
G protein-coupled receptor signaling pathway Source: BHF-UCL
High-density lipoprotein particle assembly Source: BHF-UCL
High-density lipoprotein particle clearance Source: Reactome
High-density lipoprotein particle remodeling Source: BHF-UCL
Integrin-mediated signaling pathway Source: UniProtKB
Lipid storage Source: Ensembl
Lipid transport Source: Reactome
Lipoprotein biosynthetic process Source: Ensembl
Lipoprotein metabolic process Source: GO_Central
Negative chemotaxis Source: UniProtKB
Negative regulation of cell adhesion molecule production Source: BHF-UCL
Negative regulation of cytokine production involved in immune response Source: BHF-UCL
Negative regulation of heterotypic cell-cell adhesion Source: BHF-UCL
Negative regulation of inflammatory response Source: BHF-UCL
Negative regulation of interleukin-1 beta production Source: BHF-UCL
Negative regulation of lipase activity Source: Ensembl
Negative regulation of response to cytokine stimulus Source: BHF-UCL
Negative regulation of tumor necrosis factor-mediated signaling pathway Source: BHF-UCL
Negative regulation of very-low-density lipoprotein particle remodeling Source: BHF-UCL
Peptidyl-methionine modification Source: UniProtKB
Peripheral nervous system axon regeneration Source: Ensembl
Phosphatidylcholine biosynthetic process Source: BHF-UCL
Phosphatidylcholine metabolic process Source: GO_Central
Phospholipid efflux Source: BHF-UCL
Phospholipid homeostasis Source: BHF-UCL
Platelet degranulation Source: Reactome
Positive regulation of cholesterol efflux Source: UniProtKB
Positive regulation of cholesterol esterification Source: BHF-UCL
Positive regulation of fatty acid biosynthetic process Source: GO_Central
Positive regulation of hydrolase activity Source: BHF-UCL
Positive regulation of lipid biosynthetic process Source: GO_Central
Positive regulation of lipoprotein lipase activity Source: GO_Central
Positive regulation of phagocytosis Source: UniProtKB
Positive regulation of phospholipid efflux Source: UniProtKB
Positive regulation of Rho protein signal transduction Source: UniProtKB
Positive regulation of stress fiber assembly Source: UniProtKB
Positive regulation of substrate adhesion-dependent cell spreading Source: UniProtKB
Positive regulation of triglyceride catabolic process Source: GO_Central
Post-translational protein modification Source: Reactome
Protein oxidation Source: UniProtKB
Protein stabilization Source: UniProtKB
Receptor-mediated endocytosis Source: Reactome
Regulation of Cdc42 protein signal transduction Source: BHF-UCL
Regulation of intestinal cholesterol absorption Source: GO_Central
Regulation of metabolic process Source: Reactome
Regulation of protein phosphorylation Source: Ensembl
Response to drug Source: Ensembl
Response to estrogen Source: Ensembl
Response to nutrient Source: Ensembl
Retinoid metabolic process Source: Reactome
Reverse cholesterol transport Source: BHF-UCL
Triglyceride homeostasis Source: BHF-UCL
Very-low-density lipoprotein particle remodeling Source: GO_Central
Vitamin transport Source: AgBase

Secreted

Hypoalphalipoproteinemia, primary, 2 (FHA2): A rare disorder of lipoprotein metabolism, biochemically characterized by complete or partial apoA-I deficiency and mild to severe reduction of serum high-density lipoprotein cholesterol (HDL-C). Severe hypoalphalipoproteinemia characterized by undetectable levels of apoA-I is an autosomal recessive condition, generally associated with markedly increased atherosclerotic cardiovascular disease, xanthomas and corneal opacities. Mild hypoalphalipoproteinemia characterized by half the normal plasma apoA-I and HDL-C levels is inherited as an autosomal dominant trait, may be associated with xanthomas and corneal opacities, but most patients do not have increased cardiovascular risk. APOA1 mutations may be involved in the pathogenesis of amyloid polyneuropathy-nephropathy Iowa type, also known as amyloidosis van Allen type or familial amyloid polyneuropathy type III (PubMed:3142462 and PubMed:2123470). The clinical picture is dominated by neuropathy in the early stages of the disease and nephropathy late in the course. Death is due in most cases to renal amyloidosis.
Amyloidosis 8 (AMYL8): A form of hereditary generalized amyloidosis. Clinical features include extensive visceral amyloid deposits, renal amyloidosis resulting in nephrotic syndrome, arterial hypertension, hepatosplenomegaly, cholestasis, petechial skin rash. There is no involvement of the nervous system.

Glycosylated.
Palmitoylated.
Phosphorylation sites are present in the extracellular medium.