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.

中文翻译：

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分隔的NAD +合成与消耗之间的相互作用：以PARP系列为重点。

烟酰胺腺嘌呤二核苷酸（NAD +）是氧化还原酶必不可少的辅因子，但月光也可以作为信号传递酶的底物。当通过信号传递酶用作底物时，它被消耗，必须通过挽救途径回收NAD +消费产品（即烟酰胺），以维持NAD +稳态。哺乳动物细胞中NAD +消费者的主要家族是聚ADP-核糖聚合酶（PARP）。PARPs在人类中包含17种酶，其中16种催化ADP-核糖从NAD +转移到大分子靶标（即蛋白质，也包括DNA和RNA）。由于PARPs和NAD +生物合成酶位于亚细胞内，因此出现了一个新概念，即PARPs和其他NAD +消费者的活动以分隔的方式进行调节。在这篇评论中，我讨论了NAD +代谢，