Molecular properties and regulation of NAD+ kinase (NADK).
Redox biology
confidence
Key findings
Review of NADK's evolutionary conservation, molecular properties, activation mechanisms, and role in cellular redox and metabolism; no clinical/biological endpoints reported.
View source on PubMed (PMID 36512915) ↗
- Sample size
- Not applicable (review)
- Population
- Review across archaea, bacteria, plants and mammals (molecular studies)
- Dosing
- Not applicable
- Duration
- Not applicable
- Route
- Not applicable
- Blinding
- not_reported
- Controls
- not_reported
- Drug class
- coenzyme
Full abstract
Nicotinamide adenine dinucleotide (NAD+) kinase (NADK) phosphorylates NAD+, thereby producing nicotinamide adenine dinucleotide phosphate (NADP). Both NADK genes and the NADP(H)-producing mechanism are evolutionarily conserved among archaea, bacteria, plants and mammals. In mammals, NADK is activated by phosphorylation and protein-protein interaction. Recent studies conducted using genetically altered models validate the essential role of NADK in cellular redox homeostasis and metabolism in multicellular organisms. Here, we describe the evolutionary conservation, molecular properties, and signaling mechanisms and discuss the pathophysiological significance of NADK.