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Recombinant Mouse Anti-APOB Antibody (CBAb018) (CBMAB-Ab018-LY)

The product is antibody recognizes APOB. The antibody CBAb018 immunoassay techniques such as: WB 1:500-1:2000; ICC 1:500-1:1000; FC 1:50-1:200.
See all APOB antibodies
Published Data

Summary

Host Animal
Mouse
Specificity
Human, Mouse, Rat
Clone
CBAb018
Antibody Isotype
IgG1, κ
Application
ELISA, WB, IF, IP

Basic Information

Immunogen
Amino acids 1-300 of apoB of human origin.
Host Species
Mouse
Specificity
Human, Mouse, Rat
Antibody Isotype
IgG1, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.
ApplicationNote
WB1:100-1:1,000
IP1-2 µg per 100-500 µg of total protein (1 ml of cell lysate)
IF(ICC)1:50-1:500
ELISA1:30-1:3,000

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

Format
Liquid
Buffer
PBS, 0.1% gelatin
Preservative
< 0.1% sodium azide
Concentration
0.2 mg/ml
Purity
> 95% Purity determined by SDS-PAGE.
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Full Name
Apolipoprotein B
Introduction
This gene product is the main apolipoprotein of chylomicrons and low density lipoproteins. It occurs in plasma as two main isoforms, apoB-48 and apoB-100: the former is synthesized exclusively in the gut and the latter in the liver. The intestinal and the hepatic forms of apoB are encoded by a single gene from a single, very long mRNA. The two isoforms share a common N-terminal sequence. The shorter apoB-48 protein is produced after RNA editing of the apoB-100 transcript at residue 2180 (CAA->UAA), resulting in the creation of a stop codon, and early translation termination. Mutations in this gene or its regulatory region cause hypobetalipoproteinemia, normotriglyceridemic hypobetalipoproteinemia, and hypercholesterolemia due to ligand-defective apoB, diseases affecting plasma cholesterol and apoB levels.
Entrez Gene ID
UniProt ID
Alternative Names
APOB; FLDB; LDLCQ4; apoB-100; apoB-48; apolipoprotein B
Function
Apolipoprotein B is a major protein constituent of chylomicrons (apo B-48), LDL (apo B-100) and VLDL (apo B-100). Apo B-100 functions as a recognition signal for the cellular binding and internalization of LDL particles by the apoB/E receptor.
Biological Process
Artery morphogenesis Source: Ensembl
Cellular protein metabolic process Source: Reactome
Cellular response to prostaglandin stimulus Source: Ensembl
Cellular response to tumor necrosis factor Source: Ensembl
Cholesterol efflux Source: Ensembl
Cholesterol homeostasis Source: BHF-UCL
Cholesterol metabolic process Source: BHF-UCL
Cholesterol transport Source: BHF-UCL
Chylomicron assembly Source: Reactome
Chylomicron remnant clearance Source: Reactome
Chylomicron remodeling Source: Reactome
Fertilization Source: Ensembl
Flagellated sperm motility Source: Ensembl
In utero embryonic development Source: Ensembl
Leukocyte migration Source: Reactome
Lipoprotein biosynthetic process Source: Ensembl
Lipoprotein catabolic process Source: Ensembl
Lipoprotein transport Source: GO_Central
Low-density lipoprotein particle clearance Source: BHF-UCL
Low-density lipoprotein particle remodeling Source: BHF-UCL
Membrane organization Source: Reactome
Nervous system development Source: Ensembl
Positive regulation of cholesterol storage Source: BHF-UCL
Positive regulation of gene expression Source: Ensembl
Positive regulation of lipid storage Source: BHF-UCL
Positive regulation of macrophage derived foam cell differentiation Source: BHF-UCL
Post-embryonic development Source: Ensembl
Post-translational protein modification Source: Reactome
Receptor-mediated endocytosis Source: Reactome
Regulation of cholesterol biosynthetic process Source: Ensembl
Response to carbohydrate Source: Ensembl
Response to estradiol Source: Ensembl
Response to lipopolysaccharide Source: Ensembl
Response to selenium ion Source: Ensembl
Response to virus Source: UniProtKB
Retinoid metabolic process Source: Reactome
Spermatogenesis Source: Ensembl
Toll-like receptor signaling pathway Source: Reactome
Triglyceride catabolic process Source: Ensembl
Triglyceride mobilization Source: GO_Central
Very-low-density lipoprotein particle assembly Source: Reactome
Very-low-density lipoprotein particle clearance Source: Reactome
Cellular Location
Cytoplasm; Secreted; Lipid droplet
Involvement in disease
Hypobetalipoproteinemia, familial, 1 (FHBL1): The disease is caused by variants affecting the gene represented in this entry. Most cases of FHBL1 result from nonsense mutations in the APOB gene that lead to a premature stop codon, which generate prematurely truncated apo B protein products (PubMed:21981844). A disorder of lipid metabolism characterized by less than 5th percentile age- and sex-specific levels of low density lipoproteins, and dietary fat malabsorption. Clinical presentation may vary from no symptoms to severe gastrointestinal and neurological dysfunction similar to abetalipoproteinemia.
Hypercholesterolemia, familial, 2 (FHCL2): A form of hypercholesterolemia, a disorder of lipoprotein metabolism characterized by elevated serum low-density lipoprotein (LDL) cholesterol levels, which result in excess deposition of cholesterol in tissues and leads to xanthelasma, xanthomas, accelerated atherosclerosis and increased risk of premature coronary heart disease. FHCL2 inheritance is autosomal dominant.
PTM
Palmitoylated; structural requirement for proper assembly of the hydrophobic core of the lipoprotein particle.

Johannesen, C. D. L., Mortensen, M. B., Langsted, A., & Nordestgaard, B. G. (2021). Apolipoprotein B and non-HDL cholesterol better reflect residual risk than LDL cholesterol in statin-treated patients. Journal of the American College of Cardiology, 77(11), 1439-1450.

Tian, M., Li, R., Shan, Z., Wang, D. W., Jiang, J., & Cui, G. (2019). Comparison of Apolipoprotein B/A1 ratio, Framingham risk score and TC/HDL-c for predicting clinical outcomes in patients undergoing percutaneous coronary intervention. Lipids in health and disease, 18(1), 1-9.

Sniderman, A. D., Thanassoulis, G., Glavinovic, T., Navar, A. M., Pencina, M., Catapano, A., & Ference, B. A. (2019). Apolipoprotein B particles and cardiovascular disease: a narrative review. JAMA cardiology, 4(12), 1287-1295.

Yan, X., Yao, M., Wen, X., Zhu, Y., Zhao, E., Qian, X., ... & Lu, F. (2019). Elevated apolipoprotein B predicts poor postsurgery prognosis in patients with hepatocellular carcinoma. OncoTargets and therapy, 12, 1957.

Cao, J., Steffen, B. T., Guan, W., Remaley, A. T., McConnell, J. P., Palamalai, V., & Tsai, M. Y. (2018). A comparison of three apolipoprotein B methods and their associations with incident coronary heart disease risk over a 12-year follow-up period: The Multi-Ethnic Study of Atherosclerosis. Journal of clinical lipidology, 12(2), 300-304.

Ma, M. Z., Yuan, S. Q., Chen, Y. M., & Zhou, Z. W. (2018). Preoperative apolipoprotein B/apolipoprotein A1 ratio: a novel prognostic factor for gastric cancer. OncoTargets and therapy, 11, 2169.

Lee, J. Y., Kang, M. J., Choi, J. Y., Park, J. S., Park, J. K., Lee, E. Y., ... & Song, Y. W. (2018). Apolipoprotein B binds to enolase-1 and aggravates inflammation in rheumatoid arthritis. Annals of the rheumatic diseases, 77(10), 1480-1489.

Viney, N. J., Yeang, C., Yang, X., Xia, S., Witztum, J. L., & Tsimikas, S. (2018). Relationship between “LDL-C”, estimated true LDL-C, apolipoprotein B-100, and PCSK9 levels following lipoprotein (a) lowering with an antisense oligonucleotide. Journal of clinical lipidology, 12(3), 702-710.

Nass, K. J., van den Berg, E. H., Faber, K. N., Schreuder, T. C., Blokzijl, H., & Dullaart, R. P. (2017). High prevalence of apolipoprotein B dyslipoproteinemias in non-alcoholic fatty liver disease: The lifelines cohort study. Metabolism, 72, 37-46.

Shapiro, M. D., & Fazio, S. (2017). Apolipoprotein B-containing lipoproteins and atherosclerotic cardiovascular disease. F1000Research, 6.

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

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