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。
TXNRD1 Rabbit mAb
- 产品详情
- 实验流程
- 背景知识
Application 
| WB, IHC-P, IHC-F, FC, IP |
|---|---|
| Primary Accession | Q16881 |
| Reactivity | Rat, Human, Mouse |
| Host | Rabbit |
| Clonality | Monoclonal Antibody |
| Isotype | IgG |
| Conjugate | Unconjugated |
| Purification | Affinity Purified |
| Calculated MW | 70906 Da |
| Gene ID | 7296 |
|---|---|
| Other Names | TXNRD1 |
| Dilution | WB~~1:1000-1:5000 IHC-P~~1:50~200 IHC-F~~N/A FC~~1:100-1:500 IP~~1:10-1:100 |
| Format | Liquid in 50mM Tris-Glycine(pH 7.4), 0.15M NaCl, 40%Glycerol, 0.01% sodium azide and 0.05% BSA. |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| Name | TXNRD1 (HGNC:12437) |
|---|---|
| Synonyms | GRIM12, KDRF |
| Function | Reduces disulfide protein thioredoxin (Trx) to its dithiol- containing form (PubMed:8577704). Homodimeric flavoprotein involved in the regulation of cellular redox reactions, growth and differentiation. A selenocysteine residue at the C-terminal active site is essential for catalysis (Probable). Also has reductase activity on hydrogen peroxide (H2O2) (PubMed:10849437). |
| Cellular Location | [Isoform 1]: Cytoplasm [Isoform 5]: Cytoplasm |
| Tissue Location | [Isoform 1]: Expressed predominantly in Leydig cells (at protein level). Also expressed in ovary, spleen, heart, liver, kidney and pancreas and in a number of cancer 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
Isoform 1 may possess glutaredoxin activity as well as thioredoxin reductase activity and induces actin and tubulin polymerization, leading to formation of cell membrane protrusions. Isoform 4 enhances the transcriptional activity of estrogen receptors alpha and beta while isoform 5 enhances the transcriptional activity of the beta receptor only. Isoform 5 also mediates cell death induced by a combination of interferon-beta and retinoic acid.
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