癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
SNAI1 Antibody (N-term D24)
Purified Rabbit Polyclonal Antibody (Pab)
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Application 
| WB, IHC-P, E |
|---|---|
| Primary Accession | O95863 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 29083 Da |
| Antigen Region | 9-39 aa |
| Gene ID | 6615 |
|---|---|
| Other Names | Zinc finger protein SNAI1, Protein snail homolog 1, Protein sna, SNAI1, SNAH |
| Target/Specificity | This SNAI1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 9-39 amino acids from the N-terminal region of human SNAI1. |
| Dilution | WB~~1：1000 IHC-P~~N/A E~~Use at an assay dependent concentration. |
| Format | Purified polyclonal antibody supplied in PBS with 0.05% (V/V) Proclin 300. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | SNAI1 Antibody (N-term D24) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | SNAI1 |
|---|---|
| Synonyms | SNAH |
| Function | Involved in induction of the epithelial to mesenchymal transition (EMT), formation and maintenance of embryonic mesoderm, growth arrest, survival and cell migration (PubMed:10655587, PubMed:15647282, PubMed:20389281, PubMed:20562920, PubMed:21952048, PubMed:25827072). Binds to 3 E-boxes of the E-cadherin/CDH1 gene promoter and to the promoters of CLDN7 and KRT8 and, in association with histone demethylase KDM1A which it recruits to the promoters, causes a decrease in dimethylated H3K4 levels and represses transcription (PubMed:10655587, PubMed:20389281, PubMed:20562920). The N-terminal SNAG domain competes with histone H3 for the same binding site on the histone demethylase complex formed by KDM1A and RCOR1, and thereby inhibits demethylation of histone H3 at 'Lys-4' (in vitro) (PubMed:20389281, PubMed:21300290, PubMed:23721412). During EMT, involved with LOXL2 in negatively regulating pericentromeric heterochromatin transcription (PubMed:16096638). SNAI1 recruits LOXL2 to pericentromeric regions to oxidize histone H3 and repress transcription which leads to release of heterochromatin component CBX5/HP1A, enabling chromatin reorganization and acquisition of mesenchymal traits (By similarity). Associates with EGR1 and SP1 to mediate tetradecanoyl phorbol acetate (TPA)-induced up-regulation of CDKN2B, possibly by binding to the CDKN2B promoter region 5'-TCACA-3 (PubMed:20121949). In addition, may also activate the CDKN2B promoter by itself (PubMed:20121949). |
| Cellular Location | Nucleus. Cytoplasm. Note=Once phosphorylated (probably on Ser-107, Ser-111, Ser-115 and Ser-119) it is exported from the nucleus to the cytoplasm where subsequent phosphorylation of the destruction motif and ubiquitination involving BTRC occurs. |
| Tissue Location | Expressed in a variety of tissues with the highest expression in kidney. Expressed in mesenchymal and epithelial cell lines. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
The Drosophila embryonic protein snail is a zinc finger transcriptional repressor which downregulates the expression of ectodermal genes within the mesoderm. The nuclear protein encoded by this gene is structurally similar to the Drosophila snail protein, and is also thought to be critical for mesoderm formation in the developing embryo.
REFERENCES
Imai, T., et al., Am. J. Pathol. 163(4):1437-1447 (2003). Yokoyama, K., et al., Int. J. Oncol. 22(4):891-898 (2003). Guaita, S., et al., J. Biol. Chem. 277(42):39209-39216 (2002). Blanco, M.J., et al., Oncogene 21(20):3241-3246 (2002). Okubo, T., et al., Cancer Res. 61(4):1338-1346 (2001).
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