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。
P27 Kip1 (1A7) Mouse Monoclonal Antibody
P27 Kip1 (1A7) Mouse Monoclonal Antibody
- 产品详情
- 实验流程
- 背景知识
Application 
| WB, IHC |
|---|---|
| Primary Accession | P45627 |
| Reactivity | Rat, Human, Mouse |
| Host | Monoclonal, Mouse |
| Clonality | Monoclonal |
| Calculated MW | 50134 Da |
| Other Names | Glutamine synthetase, GS, 6.3.1.2, glnA {ECO:0000303|PubMed:1359838} |
|---|---|
| Dilution | WB~~1:1000 IHC~~1:100~500 |
| Storage Conditions | -20℃ |
| Name | glnA {ECO:0000303|PubMed:1359838} |
|---|---|
| Function | Glutamine synthetase (GS) is an unusual multitasking protein that functions as an enzyme, a transcription coregulator, and a chaperone in ammonium assimilation and in the regulation of genes involved in nitrogen metabolism. It catalyzes the ATP-dependent biosynthesis of glutamine from glutamate and ammonia. Feedback- inhibited GlnA also interacts with and regulates the activity of the transcriptional regulator TnrA. During nitrogen limitation, TnrA is in its DNA-binding active state and turns on the transcription of genes required for nitrogen assimilation. Under conditions of nitrogen excess, feedback-inhibited GlnA forms a stable complex with TnrA, which inhibits its DNA-binding activity. In contrast, feedback-inhibited GlnA acts as a chaperone to stabilize the DNA-binding activity of GlnR, which represses the transcription of nitrogen assimilation genes. |
| Cellular Location | Cytoplasm {ECO:0000250|UniProtKB:P12425}. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Cyclin dependent kinase inhibitor 1B(CDKN1B) Homo sapiens This gene encodes a cyclin-dependent kinase inhibitor, which shares a limited similarity with CDK inhibitor CDKN1A/p21. The encoded protein binds to and prevents the activation of cyclin E-CDK2 or cyclin D-CDK4 complexes, and thus controls the cell cycle progression at G1. The degradation of this protein, which is triggered by its CDK dependent phosphorylation and subsequent ubiquitination by SCF complexes, is required for the cellular transition from quiescence to the proliferative state.
终于等到您。ABCEPTA（百远生物）抗体产品。
点击下方“我要评价 ”按钮提交您的反馈信息，您的反馈和评价是我们最宝贵的财富之一,
我们将在1-3个工作日内处理您的反馈信息。
如有疑问，联系：0512-88856768 tech-china@abcepta.com.
