人 NADK 抗体对
01AB01242
NAD kinase (NADK) is a critical enzyme that phosphorylates nicotinamide adenine dinucleotide (NAD⁺) to produce NADP⁺, which is subsequently reduced to NADPH, a vital cofactor in anabolic reactions and redox homeostasis. Structurally, NADK contains conserved domains including the GGDG motif, NE/D short motif, and a conserved region II, which are essential for NAD⁺ binding and catalytic activity. Key residues such as D185, N280, E281, T321, and Y323 play crucial roles in substrate recognition and phosphorylation. Mammalian NADK typically forms a homotetramer, with phosphorylation sites regulated by kinases like Akt and PKC, enabling dynamic control of its activity. NADK's function is evolutionarily conserved across species, underscoring its fundamental role in cellular metabolism. Clinically, mutations in NADK or its mitochondrial isoform NADK2 cause severe metabolic and developmental disorders, including mitochondrial dysfunction, hyperlysinemia, and neurological defects. Additionally, NADK dysregulation is linked to cancer progression due to enhanced NADP(H)-dependent antioxidant defenses.
| 规格 | 起售价 |
|---|---|
| 登录后可查看 | |
技术参数
- 靶点基因名
- NADK
- 蛋白别名
- NAD kinase; NADK
- UniProt
- O95544
- 物种
- Human
产品详情
- 靶点名称
- NADK
- 蛋白名称
- NAD kinase
- 蛋白别名
- NAD kinase; Poly(P)/ATP NAD kinase
- 靶点基因名
- NADK
- UniProt
- O95544
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
NAD kinase (NADK) is a critical enzyme that phosphorylates nicotinamide adenine dinucleotide (NAD⁺) to produce NADP⁺, which is subsequently reduced to NADPH, a vital cofactor in anabolic reactions and redox homeostasis. Structurally, NADK contains conserved domains including the GGDG motif, NE/D short motif, and a conserved region II, which are essential for NAD⁺ binding and catalytic activity. Key residues such as D185, N280, E281, T321, and Y323 play crucial roles in substrate recognition and phosphorylation. Mammalian NADK typically forms a homotetramer, with phosphorylation sites regulated by kinases like Akt and PKC, enabling dynamic control of its activity. NADK's function is evolutionarily conserved across species, underscoring its fundamental role in cellular metabolism. Clinically, mutations in NADK or its mitochondrial isoform NADK2 cause severe metabolic and developmental disorders, including mitochondrial dysfunction, hyperlysinemia, and neurological defects. Additionally, NADK dysregulation is linked to cancer progression due to enhanced NADP(H)-dependent antioxidant defenses.