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。
Snk Polyclonal Antibody
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Application 
| WB |
|---|---|
| Primary Accession | Q9NYY3 |
| Reactivity | Human, Mouse, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 78237 Da |
| Gene ID | 10769 |
|---|---|
| Other Names | PLK2; SNK; Serine/threonine-protein kinase PLK2; Polo-like kinase 2; PLK-2; hPlk2; Serine/threonine-protein kinase SNK; hSNK; Serum-inducible kinase |
| Dilution | WB~~Western Blot: 1/500 - 1/2000. ELISA: 1/40000. Not yet tested in other applications. |
| Format | Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.09% (W/V) sodium azide. |
| Storage Conditions | -20℃ |
| Name | PLK2 |
|---|---|
| Synonyms | SNK |
| Function | Tumor suppressor serine/threonine-protein kinase involved in synaptic plasticity, centriole duplication and G1/S phase transition. Polo-like kinases act by binding and phosphorylating proteins that are already phosphorylated on a specific motif recognized by the POLO box domains. Phosphorylates CPAP, NPM1, RAPGEF2, RASGRF1, SNCA, SIPA1L1 and SYNGAP1. Plays a key role in synaptic plasticity and memory by regulating the Ras and Rap protein signaling: required for overactivity-dependent spine remodeling by phosphorylating the Ras activator RASGRF1 and the Rap inhibitor SIPA1L1 leading to their degradation by the proteasome. Conversely, phosphorylates the Rap activator RAPGEF2 and the Ras inhibitor SYNGAP1, promoting their activity. Also regulates synaptic plasticity independently of kinase activity, via its interaction with NSF that disrupts the interaction between NSF and the GRIA2 subunit of AMPARs, leading to a rapid rundown of AMPAR-mediated current that occludes long term depression. Required for procentriole formation and centriole duplication by phosphorylating CPAP and NPM1, respectively. Its induction by p53/TP53 suggests that it may participate in the mitotic checkpoint following stress. |
| Cellular Location | Cytoplasm, cytoskeleton, microtubule organizing center, centrosome, centriole. Cell projection, dendrite Note=Localizes to centrosomes during early G1 phase where it only associates to the mother centriole and then distributes equally to both mother and daughter centrioles at the onset of S phase |
| Tissue Location | Expressed at higher level in the fetal lung, kidney, spleen and heart. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Tumor suppressor serine/threonine-protein kinase involved in synaptic plasticity, centriole duplication and G1/S phase transition. Polo-like kinases act by binding and phosphorylating proteins are that already phosphorylated on a specific motif recognized by the POLO box domains. Phosphorylates CENPJ, NPM1, RAPGEF2, RASGRF1, SNCA, SIPA1L1 and SYNGAP1. Plays a key role in synaptic plasticity and memory by regulating the Ras and Rap protein signaling: required for overactivity-dependent spine remodeling by phosphorylating the Ras activator RASGRF1 and the Rap inhibitor SIPA1L1 leading to their degradation by the proteasome. Conversely, phosphorylates the Rap activator RAPGEF2 and the Ras inhibitor SYNGAP1, promoting their activity. Also regulates synaptic plasticity independently of kinase activity, via its interaction with NSF that disrupts the interaction between NSF and the GRIA2 subunit of AMPARs, leading to a rapid rundown of AMPAR-mediated current that occludes long term depression. Required for procentriole formation and centriole duplication by phosphorylating CENPJ and NPM1, respectively. Its induction by p53/TP53 suggests that it may participate in the mitotic checkpoint following stress.
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