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。
Anti-Gephyrin Antibody
Our Anti-Gephyrin rabbit polyclonal primary antibody from PhosphoSolutions is produced in-house. It
- 产品详情
- 实验流程
- 背景知识
Application 
| WB |
|---|---|
| Primary Accession | Q03555 |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | IgG |
| Calculated MW | 83266 Da |
| Gene ID | 64845 |
|---|---|
| Other Names | Domain E antibody, Domain G antibody, GEPH antibody, GEPH_HUMAN antibody, GPH antibody, GPHN antibody, GPHRYN antibody, KIAA1385 antibody, Molybdopterin molybdenumtransferase antibody, MPT adenylyltransferase antibody, MPT Mo-transferase antibody |
| Target/Specificity | In neuronal tissue, gephyrin is a scaffolding protein that self assembles in a complex, flat submembraneous lattice that inhibits mobility of the glycine receptors (GlyR) and GABA-A receptors (GABA-A-R) causing clustering at post synaptic sites (Groeneweg et al, 2018). In non-neuronal tissue gephyrin plays a critical role in the molybdendum cofactor (MoCo) biosynthesis of essential life molybdoenzymes, like sulphite oxidase (Groeneweg et al, 2018). Three functional domains have been identified in gephyrin: the stable, structural G and E domains, and the C domain which is intrinsically unstructured leading to multiple isoforms (108, 105, 102, 98, 90 kDa) (Kawasaki, et al 1997). The 93 kDa protein predominantly expressed in the brain and located in the plasma membrane, has a 10X stronger affinity for the GlyR than the GABA-A-R. Gephyrin’s flexibility to change its size and molecular density is directly correlated to its high affinity to the GlyR-β subunit, and is required for anchoring and accurate clustering of GlyRs at post synaptic sites and microtubule transport chains (Greoneweg et al, 2018). A consistent parameter in the pathogenesis of Alzheimers Disease shows a decrease of inhibitory GABAergic synapses and gephyrin, and increased levels of an insoluble 37 kDa gephyrin fragment not detected in healthy, non-AD models (Kiss et al, 2016). |
| Dilution | WB~~1:1000 |
| Format | Antigen Affinity Purified from Serum |
| Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | Anti-Gephyrin Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| Shipping | Blue Ice |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
In neuronal tissue, gephyrin is a scaffolding protein that self assembles in a complex, flat submembraneous lattice that inhibits mobility of the glycine receptors (GlyR) and GABA-A receptors (GABA-A-R) causing clustering at post synaptic sites (Groeneweg et al, 2018). In non-neuronal tissue gephyrin plays a critical role in the molybdendum cofactor (MoCo) biosynthesis of essential life molybdoenzymes, like sulphite oxidase (Groeneweg et al, 2018). Three functional domains have been identified in gephyrin: the stable, structural G and E domains, and the C domain which is intrinsically unstructured leading to multiple isoforms (108, 105, 102, 98, 90 kDa) (Kawasaki, et al 1997). The 93 kDa protein predominantly expressed in the brain and located in the plasma membrane, has a 10X stronger affinity for the GlyR than the GABA-A-R. Gephyrin’s flexibility to change its size and molecular density is directly correlated to its high affinity to the GlyR-β subunit, and is required for anchoring and accurate clustering of GlyRs at post synaptic sites and microtubule transport chains (Greoneweg et al, 2018). A consistent parameter in the pathogenesis of Alzheimers Disease shows a decrease of inhibitory GABAergic synapses and gephyrin, and increased levels of an insoluble 37 kDa gephyrin fragment not detected in healthy, non-AD models (Kiss et al, 2016).
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