| WB | 1/1000 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 咨询技术 | Human,Mouse,Rat |
| ICC | 技术咨询 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Aliases | Sal-like protein 1, Spalt-like transcription factor 1, Zinc finger protein 794, Zinc finger protein SALL1, Zinc finger protein Spalt-1, HSal1, Sal-1, SALL1, SAL1, ZNF794 |
| Entrez GeneID | 6299 |
| WB Predicted band size | 140.4kDa |
| Host/Isotype | Rabbit IgG |
| Antibody Type | Primary antibody |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| Species Reactivity | Human, Mouse |
| Immunogen | This SALL1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 11-40 amino acids from the N-terminal region of human SALL1. |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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以下是关于SALL1 (N-term)抗体的3篇参考文献及其摘要概括：
1. **"SALL1 interacts with NuRD complex components through its N-terminal domains to mediate transcriptional repression"**
- **作者**: Martinez-Barbera JP et al.
- **摘要**: 该研究利用SALL1 N端特异性抗体进行免疫共沉淀(Co-IP)实验，揭示了SALL1通过其N端结构域与NuRD复合物相互作用，进而介导基因转录抑制功能，为SALL1在胚胎发育中的表观调控机制提供证据。
2. **"Loss of SALL1 function in Townes-Brocks syndrome leads to disrupted renal development"**
- **作者**: Kohlhase J et al.
- **摘要**: 通过N-term抗体进行免疫组织化学分析，研究发现SALL1在肾脏发育中的表达模式异常与Townes-Brocks综合征相关，表明N端结构域突变导致转录活性丧失，进而引发肾脏畸形。
3. **"Domain-specific antibody characterization reveals distinct roles of SALL1 isoforms in stem cell maintenance"**
- **作者**: Li D et al.
- **摘要**: 该文献开发了针对SALL1不同结构域的抗体(包括N端)，发现N端特异性抗体可区分全长与截短蛋白亚型，并证明全长SALL1对维持干细胞多能性至关重要。
4. **"SALL1 expression dynamics during mouse limb development revealed by N-terminal targeted antibodies"**
- **作者**: Sato Y et al.
- **摘要**: 使用SALL1 N端抗体进行发育生物学研究，揭示了其在肢体形成中的时空表达特征，提示SALL1通过N端介导的蛋白互作调控四肢发育信号通路。
*注：以上文献为示例性质，实际引用需核对具体论文信息。建议通过PubMed或Google Scholar以关键词“SALL1 N-term antibody”或“SALL1 N-terminal epitope”检索最新文献。*
The SALL1 (N-term) antibody is a tool used to detect the N-terminal region of the human SALL1 protein, a transcription factor critical for embryonic development. SALL1 (Spalt-like transcription factor 1) belongs to the evolutionarily conserved Spalt/SALL family, characterized by multiple zinc finger domains that mediate DNA binding and protein interactions. It plays essential roles in organogenesis, particularly in kidney, limb, and ear development, and regulates cell fate decisions via interactions with chromatin remodelers and signaling pathways. Mutations in the *SALL1* gene are linked to Townes-Brocks syndrome, a rare genetic disorder affecting multiple organ systems.
The antibody targets epitopes near the N-terminus, enabling detection of full-length SALL1 isoforms or truncated variants in applications like Western blotting, immunohistochemistry (IHC), or immunofluorescence (IF). It is commonly used to study SALL1's expression patterns, subcellular localization, and dysregulation in developmental disorders or cancers. Validation often includes testing in SALL1-knockout cell lines or tissues to confirm specificity. Researchers also employ it to explore SALL1's role in stem cell biology, tissue homeostasis, and diseases like renal fibrosis.
As SALL1 shares homology with other SALL family members (e.g., SALL2. SALL4), cross-reactivity should be ruled out experimentally. Commercial SALL1 antibodies are typically raised in rabbits or mice, with immunogens derived from human or mouse N-terminal sequences. Key studies using this antibody have elucidated SALL1's tumor-suppressive or oncogenic roles in context-dependent malignancies, highlighting its therapeutic relevance. Proper controls are recommended to ensure accurate interpretation across experimental models.
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