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CDK5 Antibody
CDK5 Antibody
- 中文名称：
- CDK5 Antibody
- 英文名称：
- CDK5 Antibody
- 品牌：
- AAA Biotech
- 品牌介绍：
- AAA Biotech专注于为全球生命科学研究提供高品质的蛋白质研究工具，核心产品包括经严格验证的抗体、重组蛋白及ELISA试剂盒。
- 货号：
- AAA111277
- 规格：
- 0.1 mg|0.1 mL (AF647)|0.1 mL (AF594)|0.1 mL (HRP)|0.1 mL (PE)
- 保存建议：
- 请按照说明书指示
- 货期：
- 6-8周
- 来源宿主：
- Mouse
- 反应种属：
- Human
- 应用：
- ICC (Immunocytochemistry), WB (Western Blot)
- 免责声明：
- *本产品仅供科研实验使用，不得用于临床诊断。*
- 其他：
克隆性:Monoclonal
同型:IgG1
克隆号:N/A
特异性:This antibody detects endogenous levels CDK5(N-terminus) and does not cross-react with related proteins.
纯度:Affinity purified
形式：Purified in buffer containing 0.1M Tris-Glycine (pH 7.4, 150 mM NaCl) with 0.2% sodium azide, 50%, glycerol
浓度：N/A
- 说明书：
UniPort Summary Function: Probably involved in the control of the cell cycle. Interacts with D1 and D3-type G1 cyclins. Can phosphorylate histone H1, tau, MAP2 and NF-H and NF-M. Also interacts with p35 which activates the kinase.
Entrez Summary: Cdks (cyclin-dependent kinases) are heteromeric serine/threonine kinases that control progression through the cell cycle in concert with their regulatory subunits, the cyclins. Although there are 12 different cdk genes, only 5 have been shown to directly drive the cell cycle (Cdk1,-2,-3,-4, and-6). Following extracellular mitogenic stimuli, cyclin D gene expression is upregulated. Cdk4 forms a complex with cyclin D and phosphorylates Rb protein, leading to liberation of the transcription factor E2F. E2F induces transcription of genes including cyclins A and E, DNA polymerase and thymidine kinase. Cdk4-cyclin E complexes form and initiate G1/S transition. Subsequently, Cdk1-cyclin B complexes form and induce G2/M phase transition. Cdk1-cyclin B activation induces the breakdown of the nuclear envelope and the initiation of mitosis. Cdks are constitutively expressed and are regulated by several kinases and phosphastases, including Wee1, CDK-activating kinase and Cdc25 phosphatase. In addition, cyclin expression is induced by molecular signals at specific points of the cell cycle, leading to activation of Cdks. Tight control of Cdks is essential as misregulation can induce unscheduled proliferation, and genomic and chromosomal instability. Cdk4 has been shown to be mutated in some types of cancer, whilst a chromosomal rearrangement can lead to Cdk6 overexpression in lymphoma, leukemia and melanoma. Cdks are currently under investigation as potential targets for antineoplastic therapy, but as Cdks are essential for driving each cell cycle phase, therapeutic strategies that block Cdk activity are unlikely to selectively target tumor cells.
