抗人 ADK 抗体对
01AB01006
Adenosine kinase (ADK) is a cytoplasmic and nuclear enzyme critical for adenosine homeostasis, catalyzing the phosphorylation of adenosine to adenosine monophosphate (AMP) using ATP. This reaction regulates extracellular adenosine levels, influencing purine metabolism, DNA methylation, and adenosine receptor signaling. ADK exists in two isoforms: ADK-long (ADK-L), predominantly nuclear and associated with transcriptional regulation, and ADK-short (ADK-S), cytoplasmic and involved in metabolic clearance of adenosine. The enzyme’s activity is pivotal in maintaining cellular energy balance and modulating neuroprotective, anti-inflammatory, and anticonvulsant adenosine-mediated pathways. ADK dysfunction is linked to hypermethioninemia, a metabolic disorder characterized by elevated methionine due to impaired S-adenosylhomocysteine hydrolysis. Additionally, ADK overexpression in epilepsy reduces adenosine’s anticonvulsant effects. ADK deficiency may also contribute to liver disease and developmental abnormalities.
| 规格 | 起售价 |
|---|---|
| 登录后可查看 | |
技术参数
- 靶点基因名
- ADK
- 蛋白别名
- adenosine kinase; ADK
- UniProt
- P55263
- 物种
- Human
产品详情
- 靶点名称
- ADK
- 蛋白名称
- adenosine kinase
- 蛋白别名
- Adenosine kinase; AK; Adenosine 5'-phosphotransferase
- 靶点基因名
- ADK
- UniProt
- P55263
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Adenosine kinase (ADK) is a cytoplasmic and nuclear enzyme critical for adenosine homeostasis, catalyzing the phosphorylation of adenosine to adenosine monophosphate (AMP) using ATP. This reaction regulates extracellular adenosine levels, influencing purine metabolism, DNA methylation, and adenosine receptor signaling. ADK exists in two isoforms: ADK-long (ADK-L), predominantly nuclear and associated with transcriptional regulation, and ADK-short (ADK-S), cytoplasmic and involved in metabolic clearance of adenosine. The enzyme’s activity is pivotal in maintaining cellular energy balance and modulating neuroprotective, anti-inflammatory, and anticonvulsant adenosine-mediated pathways. ADK dysfunction is linked to hypermethioninemia, a metabolic disorder characterized by elevated methionine due to impaired S-adenosylhomocysteine hydrolysis. Additionally, ADK overexpression in epilepsy reduces adenosine’s anticonvulsant effects. ADK deficiency may also contribute to liver disease and developmental abnormalities.