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- bs-16987R-AP
- 2025年09月30日
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100ul
| 产品编号 | bs-16987R-AP |
| 英文名称 | KIAA1024 Rabbit pAb, AP conjugated |
| 中文名称 | AP标记的KIAA1024蛋白抗体 |
| 英文别名 | hypothetical protein LOC23251; UPF0258 protein KIAA1024. |
| 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 KIAA1024 |
| 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. |
| 亚细胞定位 | Membrane; Single-pass membrane protein |
| 相似性 | Belongs to the UPF0258 family. |
| 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 | Encoding more than 700 genes, chromosome 15 is made up of approximately 106 million base pairs and is about 3% of the human genome. Angelman and Prader-Willi syndromes are associated with loss of function or deletion of genes in the 15q11-q13 region. In the case of Angelman syndrome, this loss is due to inactivity of the maternal 15q11-q13 encoded UBE3A gene in the brain by either chromosomal deletion or mutation. In cases of Prader-Willi syndrome, there is a partial or complete deletion of this region from the paternal copy of chromosome 15. Tay-Sachs disease is a lethal disorder associated with mutations of the HEXA gene, which is encoded by chromosome 15. Marfan syndrome is associated with chromosome 15 through the FBN1 gene. The KIAA1024 gene product has been provisionally designated KIAA1024 pending further characterization. |
| 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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