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- bs-15559R-AP
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100ul
| 产品编号 | bs-15559R-AP |
| 英文名称 | IFT140 Rabbit pAb, AP conjugated |
| 中文名称 | AP标记的细胞纤毛内转运同源蛋白140抗体 |
| 英文别名 | Gs114; Intraflagellar transport 140 homolog(Chlamydomonas); WD and tetratricopeptide repeats protein 2; IF140_HUMAN; WDTC2. |
| 产品应用 | 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 IFT140 |
| 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. |
| 亚基 | Component of the IFT complex A (IFT-A). |
| 亚细胞定位 | Cytoplasm, cytoskeleton, cilium basal body. |
| 相似性 | Contains 9 TPR repeats. Contains 5 WD repeats. |
| 功能 | Component of the IFT complex A (IFT-A), a complex required for retrograde ciliary transport. Plays a pivotal role in proper development and function of ciliated cells. Involved in ciliogenesis and cilia maintenance. |
| 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 | IFT140 is a gene encodes one of the subunits of the intraflagellar transport (IFT) complex A. Intraflagellar transport is involved in the genesis, resorption and signaling of primary cilia. The primary cilium is a microtubule-based sensory organelle at the surface of most quiescent mammalian cells, that receives signals from its environment, such as the flow of fluid, light or odors, and transduces those signals to the nucleus. Loss of the corresponding protein in mouse results in renal cystic disease. |
| 应用 | 推荐稀释比例 |
| {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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