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100ul
| 产品编号 | bs-19515R-AP |
| 英文名称 | NUDT19 Rabbit pAb, AP conjugated |
| 中文名称 | AP标记的NUDT19蛋白抗体 |
| 英文别名 | mitochondrial; Nucleoside diphosphate-linked moiety X motif 19; nucleoside diphosphate-linked moiety X motif 19, mitochondrial; NUD19_HUMAN; nudix(nucleoside diphosphate linked moiety X)-type motif 19; Nudix motif 19; NUDT19; RP2. |
| 产品应用 | WB=1:500-2000 Not yet tested in other applications. |
| 抗体来源 | Rabbit |
| 免疫原 | KLH conjugated synthetic peptide derived from human NUDT19 |
| 亚型 | IgG |
| 纯化方法 | affinity purified by Protein A |
| 克隆类型 | Polyclonal |
| 浓度 | 1mg/ml |
| 储存液 | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| 研究领域 | Metabolism > Pathways and Processes > Cofactors, Vitamins / minerals > Co-factors Metabolism > Pathways and Processes > Metabolic signaling pathways > Lipid and lipoprotein metabolism > Hydrolysis Signal Transduction > Metabolism > Lipid metabolism Signal Transduction > Second Messenger > Lipid Messengers |
| 亚细胞定位 | Peroxisome. Mitochondrion. |
| 相似性 | Belongs to the Nudix hydrolase family. _x000D_ Contains 1 nudix hydrolase domain. |
| 功能 | Coenzyme A diphosphatase that mediates the hydrolysis of a wide range of CoA esters, including choloyl-CoA and branched-chain fatty-acyl-CoA esters. At low substrate concentrations medium and long-chain fatty-acyl-CoA esters are the primary substrates. |
| 保存条件 | Shipped at 4℃. Store at -20°C for one year. Avoid repeated freeze/thaw cycles. |
| 注意事项 | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| 应用 | 推荐稀释比例 |
| {WB} | {1:500-2000} |
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文献和实验SDS-PA gels, and subsequent detection of proteins using rabbit antisera and alkaline phosphatase-conjugated goat-anti-rabbit IgG, detected using bromo-chloro-indolyl phosphate (BCIP) and Nitro-blue tetrazolium (NBT) salts. ・
Developing Genetically Engineered Mouse Models to Study Tumor Suppression
Literature Cited Armstrong, J.F., Kaufman, M.H., Harrison, D.J., and Clarke, A.R. 1995. High‐frequency developmental abnormalities in p53‐deficient mice. Curr
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