| Concentration: | 1 mg/ml (OD 1.35 / 280 nm) |
| Source: | From fresh human plasma that has tested negative for Hepatitis C, HIV-I and HIV-II antibodies as well as Hepatitis surface antigens. |
| Purification: | Tyrosine residues in LDL were modified to nitrotyrosine to form a nitrotyrosine modified LDL. |
| Purity: | LDL purity ≥ 98% by SDS-PAGE. |
| Buffer: | In 20 mM Tris-HCl, 0.2 mM PMSF, 1 mM EDTA, 0.01 % NaN3, pH 8.5. Preserved with 50% glycerol. |
| Storage: | -20ºC for long-term and short-term storage. Aliquot to avoid repeated freezing and thawing. |
*The products are for research or manufacturing use only, not for use in human therapeutic or diagnostic applications.
Importance
Nitrotyrosine originates as tyrosine in both a free and protein-bound form which plays a key role in the process of oxidation as seen in atherosclerosis and other inflammatory conditions including active lupus, influenza, pancreatitis, ulcerative colitis, and Crohn’s disease.
The protein-bound form that is involved in atherosclerosis is attached to LDL. This molecule is then nitrated to form the biologically active nitrotyrosine. The nitrate moiety is donated by the reactive nitrating intermediate peroxynitrite (ONOO-) (Graham et al., 1993). Peroxynitrite in turn is formed from MPO-dependent oxidation of nitric oxide (NO). This MPO-mediated oxidation process occurs in a highly efficient manner in human serum (Pennathur, 2004).
Once modified, the nitrated form of LDL is then collected and consumed by macrophages via phagocytosis. While LDL− may be viewed as a circulating, atherogenic form of LDL in vivo, study has shown that tyrosine nitration and lipid peroxide together are responsible for the unfolding of α-helices inherent in LDL- formation. Oxidatively- modified low-density lipoprotein (LDL) is involved in the initiation and progression of atherosclerosis. (Hamilton et al., 2008)
Hamilton, Ryan T., Liana Asatryan, Jon T. Nilsen, Jose M. Isas, Timothy K. Gallaher, Tatsuya Sawamura, and Tzung K. Hsiai. "LDL Protein Nitration: Implication for LDL Protein Unfolding." Archives of Biochemistry and Biophysics 479.1 (2008): 1-14.
Graham A, Hogg N, Kalyanaraman B, et al. Peroxynitrite modification of low-density lipoprotein leads to recognition by the macrophage scavenger receptor. FEBS Lett 1993;330:181.
Pennathur S, Bergt C, Shao B, et al. Human atherosclerotic intima and blood of patients with established coronary artery disease contain high density lipoprotein damaged by reactive nitrogen species. J Biol Chem 2004; 279:42977.
academy biomed[A05]绵羊抗人类载脂蛋白AII多克隆抗体12A-S1a学院生物医学公司$ 155.00$ 155.00目录号数量1寄主物种： 羊浓度： 1毫克/毫升（OD 1.35 / 280 nm）抗原： 人类载脂蛋白AII纯化： 亲和纯化缓冲： 75 mM磷酸钠，75 mM NaCl，0.5 mM EDTA，0.02％NaN3，pH 7.2特异性 与人载脂蛋白AII特异性结合。免疫印迹和ELISA的稀释范围：1,000至80,000。用： 该抗体可用于检测血浆和脂蛋白中的载脂蛋白AII，免疫测定，免疫印迹，酶结合或生物素化。存储： -20°C长期保存，4°C短期保存。等分试样，以避免反复冻结和解冻。 *这些产品仅用于研究或制造用途，不能用于人体治疗或诊断应用。 重要性Apo AII占HDL的25％。它在人血浆中以77条氨基酸残基的2条相同链的二聚体形式存在，并通过二硫键连接。据报道，单链的分子量为8.7kDa（Brewer等，1972）。对小鼠的研究报道，apoAII可能具有促动脉粥样硬化作用（Warden等，1993）。然而，一项大型的欧洲前瞻性研究中的病例对照研究表明，血浆Apo AII浓度与冠心病事件密切相关（Birjmohun等，2007）。Birjmohun，RS，GM Dallinga-Thie，JA Kuivenhoven，ESg Stroes，JD Otvos，NJ Wareham，R.Luben，JJp Kastelein，K.-T. Khaw和SM Boekholdt。“载脂蛋白A-II与未来冠状动脉疾病的风险成反比。” 循环116（2007）：2029-035。Brewer，HB，SE Lux，R.Ronan和KM John。“人ApoLp-Gln-II（apoA-II），一种从高密度脂蛋白复合物中分离的载脂蛋白的氨基酸序列。” 美国国家科学院院刊69.5（1972）：1304-308。Warden，C.，C.Hedrick，J.Qiao，L.Castellani和A.Lusis。“过表达载脂蛋白A-II的转基因小鼠中的动脉粥样硬化。” 科学261（1993）：469-72。
