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- Bioss
- bs-2542R-AP
- 2025年09月30日
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100ul
| 产品编号 | bs-2542R-AP |
| 英文名称 | CLEC1 Rabbit pAb, AP conjugated |
| 中文名称 | AP标记的C型凝集素结构域家族1成员A抗体 |
| 英文别名 | CLEC-1A; C-type lectin domain family 1 member A; C-type lectin-like receptor 1; CLEC-1; 5930406N14RIK; CLEC1; CLEC1A; MGC34328; RGD1566110; C-type lectin domain family 1 member A; CLC1A_HUMAN. |
| 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 CLEC1/CLEC1A |
| 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 type II membrane protein (Probable). |
| 组织特异性 | Expressed preferentially in dendritic cells. |
| 相似性 | Contains 1 C-type lectin domain. |
| 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 the C-type lectin/C-type lectin-like domain (CTL/CTLD) superfamily. Members of this family share a common protein fold and have diverse functions, such as cell adhesion, cell-cell signalling, glycoprotein turnover, and roles in inflammation and immune response. The encoded protein may play a role in regulating dendritic cell function. Alternative splice variants have been described but their biological nature has not been determined. This gene is closely linked to other CTL/CTLD superfamily members on chromosome 12p13 in the natural killer gene complex region. [provided by RefSeq] |
| 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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