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Mouse Anti-APOA5 Recombinant Antibody (E12) (CBMAB-A3151-YC)

Provided herein is a Mouse monoclonal antibody against Human Apolipoprotein A5. The antibody can be used for immunoassay techniques, such as WB, ICC, IHC-P, IHC-Fr, ELISA, IP, IF, FC.
See all APOA5 antibodies
Published Data

Summary

Host Animal
Mouse
Specificity
Mouse
Clone
E12
Antibody Isotype
IgG1, κ
Application
ELISA, WB, IF, IP

Basic Information

Immunogen
Amino acids 69-368 mapping at the C-terminus of apoA-V of mouse origin.
Host Species
Mouse
Specificity
Mouse
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
Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Apolipoprotein A5
Introduction
APOA5 is an apolipoprotein that plays an important role in regulating the plasma triglyceride levels, a major risk factor for coronary artery disease. It is a component of high density lipoprotein and is highly similar to a rat protein that is upregulated
Entrez Gene ID
UniProt ID
Alternative Names
Apolipoprotein A5; Regeneration-Associated Protein 3; Apolipoprotein A-V; Apo-AV; RAP3; Apolipoprotein A-V Precursor Variant 3; ApoA-V; APOAV;
Function
Minor apolipoprotein mainly associated with HDL and to a lesser extent with VLDL. May also be associated with chylomicrons. Important determinant of plasma triglyceride (TG) levels by both being a potent stimulator of apo-CII lipoprotein lipase (LPL) TG hydrolysis and an inhibitor of the hepatic VLDL-TG production rate (without affecting the VLDL-apoB production rate) (By similarity). Activates poorly lecithin:cholesterol acyltransferase (LCAT) and does not enhance efflux of cholesterol from macrophages. Binds heparin (PubMed:17326667).
Biological Process
Acylglycerol homeostasis Source: BHF-UCL
Cellular protein metabolic process Source: Reactome
Cholesterol biosynthetic process Source: GO_Central
Cholesterol efflux Source: GO_Central
Cholesterol homeostasis Source: BHF-UCL
High-density lipoprotein particle assembly Source: GO_Central
Lipid transport Source: BHF-UCL
Lipoprotein metabolic process Source: GO_Central
Phosphatidylcholine metabolic process Source: GO_Central
Phospholipid efflux Source: GO_Central
Positive regulation of cholesterol esterification Source: GO_Central
Positive regulation of fatty acid biosynthetic process Source: BHF-UCL
Positive regulation of lipid biosynthetic process Source: GO_Central
Positive regulation of lipid catabolic process Source: BHF-UCL
Positive regulation of lipoprotein lipase activity Source: BHF-UCL
Positive regulation of receptor-mediated endocytosis Source: BHF-UCL
Positive regulation of triglyceride catabolic process Source: BHF-UCL
Positive regulation of very-low-density lipoprotein particle remodeling Source: BHF-UCL
Post-translational protein modification Source: Reactome
Regulation of intestinal cholesterol absorption Source: GO_Central
Regulation of metabolic process Source: Reactome
Tissue regeneration Source: UniProtKB
Triglyceride catabolic process Source: BHF-UCL
Triglyceride homeostasis Source: BHF-UCL
Triglyceride metabolic process Source: BHF-UCL
Very-low-density lipoprotein particle remodeling Source: GO_Central
Cellular Location
Trans-Golgi network; Secreted; Early endosome; Late endosome. In the presence of SORL1, internalized to early endosomes, sorted in a retrograde fashion to late endosomes, from which a portion is sent to lysosomes and degradation, another portion is sorted to the trans-Golgi network.
Involvement in disease
Hypertriglyceridemia, familial (FHTR): A common inherited disorder in which the concentration of very low density lipoprotein (VLDL) is elevated in the plasma. This leads to increased risk of heart disease, obesity, and pancreatitis.
Hyperlipoproteinemia 5 (HLPP5): Characterized by increased amounts of chylomicrons and very low density lipoprotein (VLDL) and decreased low density lipoprotein (LDL) and high density lipoprotein (HDL) in the plasma after a fast. Numerous conditions cause this phenotype, including insulin-dependent diabetes mellitus, contraceptive steroids, alcohol abuse, and glycogen storage disease type 1A (GSD1A).
PTM
Phosphorylated by FAM20C in the extracellular medium.

Li, R., Zhu, W., Huang, P., Yang, Y., Luo, F., Dai, W., ... & Huang, X. (2021). Olanzapine leads to nonalcoholic fatty liver disease through the apolipoprotein A5 pathway. Biomedicine & Pharmacotherapy, 141, 111803.

Huang, X., Zhang, Y., Zhu, W., Huang, P., Xiao, J., Yang, Y., ... & Wu, R. (2021). Olanzapine inhibits hepatic apolipoprotein A5 secretion inducing hypertriglyceridemia in schizophrenia patients and mice. medRxiv.

Su, X., Weng, S., & Peng, D. (2020). New Insights into Apolipoprotein A5 and the Modulation of Human Adipose-derived Mesenchymal Stem Cells Adipogenesis. Current molecular medicine, 20(2), 144-156.

Dai, W., Zhang, Z., Yao, C., & Zhao, S. (2019). Emerging evidences for the opposite role of apolipoprotein C3 and apolipoprotein A5 in lipid metabolism and coronary artery disease. Lipids in health and disease, 18(1), 1-7.

Tao, Y. C., Wang, M. L., Wu, D. B., Luo, C., Tang, H., & Chen, E. Q. (2019). Apolipoprotein A5 alleviates LPS/D-GalN-induced fulminant liver failure in mice by inhibiting TLR4-mediated NF-κB pathway. Journal of translational medicine, 17(1), 151.

Gunawan, A., Anggrela, D., Listyarini, K., Abuzahra, M. A., Jakaria, J., Yamin, M., ... & Sumantri, C. (2018). Identification of Single Nucleotide Polymorphism and Pathway Analysis of Apolipoprotein A5 (APOA5) related to fatty acid traits in Indonesian sheep. Tropical Animal Science Journal, 41(3), 165-173.

Su, X., Kong, Y., & Peng, D. Q. (2018). New insights into apolipoprotein A5 in controlling lipoprotein metabolism in obesity and the metabolic syndrome patients. Lipids in health and disease, 17(1), 1-10.

Lin, M. J., Dai, W., Scott, M. J., Li, R., Zhang, Y. Q., Yang, Y., ... & Huang, X. S. (2017). Metformin improves nonalcoholic fatty liver disease in obese mice via down-regulation of apolipoprotein A5 as part of the AMPK/LXRα signaling pathway. Oncotarget, 8(65), 108802.

Zheng, X. Y., Yu, B. L., Xie, Y. F., Zhao, S. P., & Wu, C. L. (2017). Apolipoprotein A5 regulates intracellular triglyceride metabolism in adipocytes. Molecular medicine reports, 16(5), 6771-6779.

Zhao, S. P., Li, R., Dai, W., Yu, B. L., Chen, L. Z., & Huang, X. S. (2017). Xuezhikang contributes to greater triglyceride reduction than simvastatin in hypertriglyceridemia rats by up-regulating apolipoprotein A5 via the PPARα signaling pathway. PLoS one, 12(9), e0184949.

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

Custom Antibody Labeling

We also offer labeled antibodies developed using our catalog antibody products and nonfluorescent conjugates (HRP, AP, Biotin, etc.) or fluorescent conjugates (Alexa Fluor, FITC, TRITC, Rhodamine, Texas Red, R-PE, APC, Qdot Probes, Pacific Dyes, etc.).

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