[B03] Biotinylated Goat Anti-Human Apolipoprotein AI11B-G2a
|Concentration:||1 mg/ml (OD 1.35 / 280 nm)|
|Antigen:||Human Apolipoprotein AI|
|Buffer:||75 mM Sodium Phosphate, 75 mM NaCl, 0.5 mM EDTA, 0.02% NaN3, pH 7.2|
|Specificity||Specifically binds to human apo AI. Dilution for immunoblot and ELISA range: 1,000 to 80,000.|
|Use:||The antibody can be used for detection of apo AI in plasma and lipoproteins, immunoassays, immunoblots, enzyme conjugation, or biotinylation.|
|Storage:||-20°C for long-term storage, 4°C for short- term storage. Aliquot to avoid repeated freezing and thawing.|
|Form:||Freeze dried powder|
|Stabilizer:||10 mg / ml Bovine Serum Albumin.|
Freeze-dried product should be stored refrigerated until opened. After opening, restore to suggested ml volume with distilled water. If it is not completely clear after standing for 1-2 hours at room temperature, centrifuge the product. It is stable for several weeks at 4°C as an undiluted liquid. Do not use for more than one day after dilution. For extended storage after reconstitution, we suggest aliquot to avoid repeated freezing and thawing; or the addition of an equal volume of glycerol to make a final glycerol concentration of 50%, followed by storage at -20°C. The concentration of protein and buffer salts will decrease to one-half of the original after the addition of glycerol.
*These products are for research or manufacturing use only, not for use in human therapeutic or diagnostic applications.
Apo AI comprises approximately 70% of the protein moiety in HDL. It is a single polypeptide chain consisting of 243 amino acid residues without disulfide bound and with glutamic acid as the C-terminal residue and aspartic acid as the N-terminal residue. The molecular weight is reported to be 28 kDa (Brewer et al., 1978).
The roles of Apo AI in HDL function include reverse cholesterol transportation, lipid cholesterol binding, lecithin-cholesterol acyl transferase (LCAT) activation, and receptor binding, which is responsible for cholesterol esterification in plasma. Besides participate in cholesterol metabolism, Apo AI and HDL also suppress neutrophil activation, inhibit bacterial endotoxin, induce trypanosomal lysis, and other physiological activities. (Brouillette et al., 2001)
Apo AI levels may be inversely related to the risk of coronary disease. In previous research, Apo AI may affect diet-induced inflammation by either directly or indirectly altering lipid rafts. (Cheng et al., 2012)
Brewer, H. B., T. Fairwell, A. LaRue, R. Ronan, A. Houser, and T. J. Bronzert. “The amino acid sequence of human Apoa-I, an apolipoprotein isolated from high density lipoproteins.” Biochemical and Biophysical Research Communications 80.3 (1978): 623-30.
Brouillette, Christie G., G.m. Anantharamaiah, Jeffrey A. Engler, and David W. Borhani. "Structural Models of Human Apolipoprotein A-I: A Critical Analysis and Review." Biochimica Et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids (2001): 4-46.
Cheng, Andrew M., Priya Handa, Sanshiro Tateya, Jay Schwartz, Chongren Tang, Poulami Mitra, John F. Oram, Alan Chait, and Francis Kim. "Apolipoprotein A-I Attenuates Palmitate-Mediated NF-κB Activation by Reducing Toll-Like Receptor-4 Recruitment into Lipid Rafts." PLoS ONE 7.3 (2012): e33917.
|[B03]||2018||Furtado, Jeremy D.; Yamamoto, Rain; Melchior, John T.; Andraski, Allison B.; Gamez-Guerrero, Maria; Mulcahy, Patrick et al. (2018): Distinct Proteomic Signatures in 16 HDL (High-Density Lipoprotein) Subspecies. In Arterioscler Thromb Vasc Biol. 38 (12), pp. 2827–2842. DOI: 10.1161/ATVBAHA.118.311607.|
|[B03]||2012||Chen, Zhu; O'Neill, Edward A.; Meurer, Roger D.; Gagen, Karen; Luell, Silvi; Wang, Sheng-Ping et al. (2012): Reconstituted HDL elicits marked changes in plasma lipids following single-dose injection in C57Bl/6 mice. In Journal of Cardiovascular Pharmacology and Therapeutics 17 (3), pp. 315–323. DOI: 10.1177/1074248411426144.|
|[B03]||2008||Thompson, Patricia A.; Berbée, Jimmy F. P.; Rensen, Patrick C. N.; Kitchens, Richard L. (2008): Apolipoprotein A-II augments monocyte responses to LPS by suppressing the inhibitory activity of LPS-binding protein. In Innate Immunity 14 (6), pp. 365–374. DOI: 10.1177/1753425908099171.|