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Nicotinamide adenine dinucleotide (NAD + ) is an essential cofactor for redox enzymes, but also moonlights as a substrate for signaling enzymes. When used as a substrate by signaling enzymes, it is consumed, necessitating the recycling of NAD +  consumption products (i.e., nicotinamide) via a salvage pathway in order to maintain NAD +  homeostasis. A major family of NAD +  consumers in mammalian cells are poly-ADP-ribose-polymerases (PARPs). PARPs comprise a family of 17 enzymes in humans, 16 of which catalyze the transfer of ADP-ribose from NAD +  to macromolecular targets (namely, proteins, but also DNA and RNA). Because PARPs and the NAD +  biosynthetic enzymes are subcellularly localized, an emerging concept is that the activity of PARPs and other NAD +  consumers are regulated in a compartmentalized manner. In this review, I discuss NAD +  metabolism, how different subcellular pools of NAD +  are established and regulated, and how free NAD +  levels can control signaling by PARPs and redox metabolism.

Interplay between compartmentalized NAD+ synthesis and consumption: a focus on the PARP family

Interplay between compartmentalized NAD⁺ synthesis and consumption: a focus on the PARP family