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。
TXNIP Rabbit mAb
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- 背景知识
Application 
| WB, IHC-P |
|---|---|
| Primary Accession | Q9H3M7 |
| Reactivity | Rat, Human, Mouse |
| Host | Rabbit |
| Clonality | Monoclonal Antibody |
| Isotype | IgG |
| Conjugate | Unconjugated |
| Purification | Affinity Chromatography |
| Calculated MW | 43661 Da |
| Gene ID | 10628 |
|---|---|
| Other Names | TXNIP |
| Dilution | WB~~1:1000 IHC-P~~1:50~200 |
| Format | Liquid in 10mM PBS, pH 7.4, 150mM sodium chloride, 0.05% BSA, 0.02% sodium azide and 50% glycerol. |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| Name | TXNIP |
|---|---|
| Synonyms | VDUP1 |
| Function | May act as an oxidative stress mediator by inhibiting thioredoxin activity or by limiting its bioavailability (PubMed:17603038). Interacts with COPS5 and restores COPS5-induced suppression of CDKN1B stability, blocking the COPS5-mediated translocation of CDKN1B from the nucleus to the cytoplasm (By similarity). Functions as a transcriptional repressor, possibly by acting as a bridge molecule between transcription factors and corepressor complexes, and over-expression will induce G0/G1 cell cycle arrest (PubMed:12821938). Required for the maturation of natural killer cells (By similarity). Acts as a suppressor of tumor cell growth (PubMed:18541147). Inhibits the proteasomal degradation of DDIT4, and thereby contributes to the inhibition of the mammalian target of rapamycin complex 1 (mTORC1) (PubMed:21460850). |
| Cellular Location | Cytoplasm. Nucleus |
Research Areas
For Research Use Only. Not For Use In Diagnostic Procedures.
Application Protocols
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
May act as an oxidative stress mediator by inhibiting thioredoxin activity or by limiting its bioavailability. Interacts with COPS5 and restores COPS5-induced suppression of CDKN1B stability, blocking the COPS5-mediated translocation of CDKN1B from the nucleus to the cytoplasm.
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