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CDKN2A Antibody
CDKN2A Antibody
- 中文名称:
- CDKN2A Antibody
- 英文名称:
- CDKN2A 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:
- AAA304393
- 规格:
- 0.05 mL|0.1 mL|2x0.1 mL|3x0.1 mL|4x0.1 mL
- 保存建议:
- 储存在-20摄氏度
- 货期:
- 6-8周
- 来源宿主:
- Rabbit
- 反应种属:
- Human
- 应用:
- IF (Immunofluorescence), IHC (Immunohistochemistry), 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:Polyclonal
同型:N/A
克隆号:N/A
特异性:The antibody detects endogenous level of total CDKN2A protein.
纯度:Antibodies were purified by affinity purification using immunogen.
形式:Supplied at 1.0mg/mL in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
浓度:1.0 mg/ml
- 说明书:
The division cycle of eukaryotic cells is regulated by a family of protein kinases known as the cyclin-dependent kinases (CDKs). The sequential activation of individual members of this family and their consequent phosphorylation of critical substrates promotes orderly progression through the cell cycle. It has been reported that CDKN2A binds to CDK4 and inhibits the catalytic activity of the CDK4/cyclin D enzymes. CDKN2A seems to act in a regulatory feedback circuit with CDK4, D-type cyclins and retinoblastoma protein (1). The INK4 (inhibitor of cyclin-dependent kinase 4) family consists of four tumor-suppressor proteins: p15(INK4B), CDKN2A(INK4A), p18(INK4C), and p19(INK4D). While their sequences and structures are highly homologous, they show appreciable differences in conformational flexibility, stability, and aggregation tendency (2). Cell cycle arrest at the G1 checkpoint allows completion of critical macromolecular events prior to S phase. Regulators of the G1 checkpoint include an inhibitor of cyclin-dependent kinase, CDKN2AINK4; two tumor-suppressor proteins, p53 and RB and cyclin D1. CDKN2AINK4 is a tumor-suppressor protein and that genetic and epigenetic abnormalities in genes controlling the G1 checkpoint can lead to both escape from senescence and cancer formation (3).