Molecular properties and regulation of NAD+ kinase (NADK)
Shin-ichi Oka,
Allen Sam Titus,
Daniela Zablocki,
Junichi Sadoshima
Affiliations
Shin-ichi Oka
Rutgers New Jersey Medical School Department of Cell Biology and Molecular Medicine, Rutgers Biomedical and Health Sciences, Newark, NJ, 07101, USA
Allen Sam Titus
Rutgers New Jersey Medical School Department of Cell Biology and Molecular Medicine, Rutgers Biomedical and Health Sciences, Newark, NJ, 07101, USA
Daniela Zablocki
Rutgers New Jersey Medical School Department of Cell Biology and Molecular Medicine, Rutgers Biomedical and Health Sciences, Newark, NJ, 07101, USA
Junichi Sadoshima
Corresponding author. Cardiovascular Research Institute, Rutgers Biomedical and Health Science, 185 South Orange Ave., MSB G609, Newark, NJ, 07103, USA.; Rutgers New Jersey Medical School Department of Cell Biology and Molecular Medicine, Rutgers Biomedical and Health Sciences, Newark, NJ, 07101, USA
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.
