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- bs-23071R-AP
- 2026年10月14日
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100ul
| 产品编号 | bs-23071R-AP |
| 英文名称 | HES5 Rabbit pAb, AP conjugated |
| 中文名称 | AP标记的发状分裂相关增强子-5抗体 |
| 英文别名 | BHLHB38; Transcription factor HES-5; Class B basic helix-loop-helix protein 38(bHLHb38); Hairy and enhancer of split 5; HES 5; HES5 protein; MGI:104876; HES5_HUMAN. |
| 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 HES5 |
| 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 | Epigenetics and Nuclear Signaling > Transcription > Domain Families > HLH / Leucine Zipper > HLH Epigenetics and Nuclear Signaling > Transcription > Transcription Factors Neuroscience > Neurology process > Notch Pathway Stem Cells > Neural Stem Cells > Intracellular Stem Cells > Signaling Pathways > Notch > Nuclear |
| 亚基 | Transcription repression requires formation of a complex with a corepressor protein of the Groucho/TLE family. |
| 亚细胞定位 | Nucleus. |
| 组织特异性 | Expressed in fetal heart and brain tumors. |
| 相似性 | Contains 1 basic helix-loop-helix (bHLH) domain. _x000D_ Contains 1 Orange domain. |
| 功能 | Transcriptional repressor of genes that require a bHLH protein for their transcription |
| 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 | This gene encodes a member of a family of basic helix-loop-helix transcriptional repressors. The protein product of this gene, which is activated downstream of the Notch pathway, regulates cell differentiation in multiple tissues. Disruptions in the normal expression of this gene have been associated with developmental diseases and cancer. [provided by RefSeq, Dec 2008] |
| 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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