Mechanisms maintaining neuronal survival via necdin-centered protein interaction networks

Necdin与Sirt1相互作用，Sirt1使各种能量代谢相关蛋白去乙酰化，并控制下丘脑Fox01转录因子的乙酰化水平和神经肽能神经元的活性。Necdin还与SMC5/ 6复合体的几个元件相互作用，SMC5/ 6复合体参与DNA修复，并在有丝分裂后神经元DNA损伤后增强其活性。这些结果表明，necdin在参与能量代谢和DNA修复以促进神经元存活的蛋白质相互作用网络中作为枢纽蛋白。

Necdin interacted with Sirt1, which deacetylates various energy metabolism-associated proteins, and controlled the acetylation levels of the Fox01 transcription factor and neuropeptidergic neuron activities in the hypothalamus. Necdin also interacted with several elements of the SMC5/ 6 complex, which is involved in DNA repair, and enhanced its activity after DNA damage in postmitotic neurons. These results suggest that necdin serves as a hub protein in the protein interaction networks that are involved in energy metabolism and DNA repair to promote neuronal survival.