Aging An unexpected function of the oxidized form of nicotinamide adenine dinucleotide (NAD+) could underlie some effects of aging and propensity to age-related diseases. Li et al. found that the protein DBC1 (deleted in breast cancer 1) contains a domain that specifically binds NAD+. Binding of NAD+ inhibited the interaction of DBC1 with PARP1 [poly(adenosine diphosphate–ribose) polymerase 1], an enzyme important in DNA repair. Activity of PARP1 is inhibited by interaction with DBC1. Thus, the reduced abundance of NAD+ associated with aging may decrease PARP1 activity by promoting the interaction of PARP1 with DBC1. This mechanism could help explain the reported rejuvenating actions of NAD+ supplementation in older animals. Science , this issue p. [1312][1] [1]: /lookup/doi/10.1126/science.aad8242

中文翻译：

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NAD + 结合调节蛋白质相互作用

衰老 氧化形式的烟酰胺腺嘌呤二核苷酸 (NAD+) 的一个意想不到的功能可能是衰老和年龄相关疾病倾向的一些影响的基础。李等人。发现蛋白质 DBC1（在乳腺癌 1 中缺失）包含一个特异性结合 NAD+ 的结构域。NAD+ 的结合抑制了 DBC1 与 PARP1 [聚（二磷酸腺苷-核糖）聚合酶 1]（一种在 DNA 修复中很重要的酶）的相互作用。PARP1 的活性受到与 DBC1 的相互作用的抑制。因此，与衰老相关的 NAD+ 丰度降低可能通过促进 PARP1 与 DBC1 的相互作用来降低 PARP1 的活性。这种机制可以帮助解释报道的 NAD+ 补充剂对老年动物的恢复活力的作用。科学，这个问题 p。[1312][1][1]：/lookup/doi/10.1126/science.aad8242