神经退行性变中p25/Cdk5故事的续篇。
A sequel to the tale of p25/Cdk5 in neurodegeneration.
作者信息
Ikiz Burcin, Przedborski Serge
机构信息
Department of Neurology, Pathology, and Cell Biology and Center for Motor Neuron Biology and Disease, Columbia University, New York, NY 10032, USA.
出版信息
Neuron. 2008 Dec 10;60(5):731-2. doi: 10.1016/j.neuron.2008.11.020.
PMID:19081365
Abstract
p25/Cdk5 dysregulation may contribute to neurodegeneration. In this issue of Neuron, Kim et al. show that cdk5 inactivates HDAC-1, leading to cell cycle deregulation and DNA damage accumulation. This study provides further insights into the function of p25/Cdk5 in neurons and points to HDAC-1 as a target for therapeutic interventions.
摘要
p25/Cdk5功能失调可能导致神经退行性变。在本期《神经元》杂志中，金等人表明Cdk5使组蛋白去乙酰化酶-1（HDAC-1）失活，导致细胞周期失调和DNA损伤积累。这项研究进一步深入了解了p25/Cdk5在神经元中的功能，并指出HDAC-1可作为治疗干预的靶点。
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