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产品信息以Bioss网站为准
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100ul
| 产品编号 | bs-10177R-AP |
| 英文名称 | CALB1 Rabbit pAb, AP conjugated |
| 中文名称 | AP标记的钙结合蛋白D28K抗体 |
| 英文别名 | CALB1_HUMAN; Calbindin; CALB1; Calbindin D28; D-28K; Vitamin D-dependent calcium-binding protein, avian-type; CAB27; Calbindin-D28k; |
| 产品应用 | WB=1:500-2000, IHC-P=1:100-500, IHC-F=1:100-500 Not yet tested in other applications. |
| 抗体来源 | Rabbit |
| 免疫原 | KLH conjugated synthetic peptide derived from human Calbindin |
| 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 | Neuroscience > Cell Type Marker > Neuron marker > Soma marker Neuroscience > Neurotransmission > Calcium Signaling > Calcium Binding Proteins |
| 亚基 | Interacts with RANBP9. |
| 相似性 | Belongs to the calbindin family. Contains 5 EF-hand domains. |
| 功能 | Buffers cytosolic calcium. May stimulate a membrane Ca(2+)-ATPase and a 3',5'-cyclic nucleotide phosphodiesterase. |
| 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. |
| 背景资料 | Calbindin is a calcium-binding protein belonging to the troponin C superfamily. It was originally described as a 27-kD protein induced by vitamin D in the duodenum of the chick. In the brain, its synthesis is independent of vitamin-D-derived hormones. Calbindin contains 4 active calcium-binding domains, and 2 modified domains that presumably have lost their calcium-binding capacity. The neurons in brains of patients with Huntington disease are calbindin-depleted. [provided by RefSeq, Jul 2008] |
| 应用 | 推荐稀释比例 |
| {WB} | {1:500-2000} |
| {IHC-P} | {1:100-500} |
| {IHC-F} | {1:100-500} |
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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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