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在衰老过程中调节蛋白质与蛋白质相互作用的保存NAD+结合口袋

Jun Li¹, Michael S Bonkowski¹, Sébastien Moniot²

¹Department of Genetics, Paul F. Glenn Center for the Biology of Aging, Harvard Medical School, Boston, MA 02115, USA.

Science (New York, N.Y.)

|March 25, 2017

概括

尼古丁胺氨基二核酸 (NAD+) 与Nudix同源域的结合调节了对DNA修复至关重要的蛋白质相互作用. 随着年龄的增长,NAD+的下降会损害DNA的修复,但恢复NAD+水平会扭转这种下降.

科学领域:

生物化学
分子生物学
老龄化研究

背景情况:

随着年龄的增长,DNA修复效率下降,影响健康.
在蛋白质中Nudix同源域 (NHD) 的功能基本上是未知的.
尼古丁胺氨基二核酸 (NAD+) 水平随着年龄的增长而下降.

研究的目的:

阐明Nudix同质域 (NHD) 的功能.
研究NAD+在调节参与DNA修复的蛋白-蛋白相互作用中的作用.
探索衰老,NAD+下降和DNA损伤积累之间的联系.

主要方法:

研究NAD+与NHD结合的生物化学试验.
涉及DBC1和PARP1的蛋白质相互作用研究.
对老鼠进行实验,以评估NAD+水平对DNA修复的影响.

主要成果:

纽迪克斯同质域 (NHD) 被确定为调节蛋白相互作用的NAD+结合位.
与DBC1 (乳腺癌中被删除的) 的NAD+结合抑制了其与PARP1 (多) 聚合酶的相互作用.
老化小鼠的NAD+水平降低导致DBC1-PARP1抑制和DNA损伤积累的增加,这在NAD+恢复后是可逆的.

结论:

NAD+ 通过 NHD 直接调节蛋白质与蛋白质的相互作用.
在衰老过程中,NAD+-DBC1-PARP1轴是DNA修复的关键调节器.
恢复NAD+的丰富性显示出缓解与年龄相关的DNA损伤,癌症和辐射敏感性的潜力.

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