Mouse Anti-APOA5 Recombinant Antibody (CBT168) (V2LY-0625-LY3744)

Name: Mouse Anti-APOA5 Recombinant Antibody (CBT168)
SKU: V2LY-0625-LY3744
Rating: 5 (1 reviews)

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Tested Data

Mouse Anti-APOA5 Recombinant Antibody (CBT168) (V2LY-0625-LY3744) in WB

Datasheet

SDS

Request for COA

Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Host Animal

Mouse

Clone

CBT168

Application

WB, ELISA

Immunogen

Purified recombinant fragment of human ApoA-V expressed in E. Coli.

Host Species

Mouse

Specificity

Human

Antibody Isotype

IgG

Clonality

Monoclonal Antibody

Application Notes

Application	Note
ELISA	1:10,000
WB	1:500-1:2,000

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

Format

Liquid

Buffer

PBS

Preservative

Sodium azide

Concentration

Batch dependent

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.

More Infomation

Target

Full Name

Apolipoprotein A5

Entrez Gene ID

116519

UniProt ID

Q6Q788

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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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme Linked Immunospot (ELISpot)
Proteogenomic
Other Protocols

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Isotype control

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

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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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