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当正常的Cdk5发生病变时。

When good Cdk5 turns bad.

作者信息

Guo Qing

机构信息

Department of Physiology, University of Oklahoma Health Sciences Center, College of Medicine, Oklahoma City, OK 73104, USA.

出版信息

Sci Aging Knowledge Environ. 2006 Feb 8;2006(5):pe5. doi: 10.1126/sageke.2006.5.pe5.

Abstract

The cyclin-dependent kinase-5 (Cdk5) is critical to normal mammalian development and has been implicated in synaptic plasticity, learning, and memory in the adult brain. But Cdk-5 activity has also been linked to neurodegenerative diseases. Could a single protein have opposing effects? A new study shows that production of a neuronal protein capable of regulating Cdk-5 activity can turn Cdk-5 from "good" to "bad." The findings may have implications for the development and treatment of conditions like Alzheimer's disease.

摘要

细胞周期蛋白依赖性激酶5(Cdk5)对哺乳动物的正常发育至关重要,并且与成人大脑的突触可塑性、学习和记忆有关。但Cdk-5的活性也与神经退行性疾病有关。一种蛋白质会产生相反的作用吗?一项新的研究表明,一种能够调节Cdk-5活性的神经元蛋白的产生可以使Cdk-5从“好”变“坏”。这些发现可能对阿尔茨海默病等疾病的发展和治疗具有启示意义。

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