When good Cdk5 turns bad.
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.
Guo
Qing
Q
Department of Physiology, University of Oklahoma Health Sciences Center, College of Medicine, Oklahoma City, OK 73104, USA. qing-guo@ouhsc.edu
D000544:Alzheimer Disease / Q000503:physiopathology*; D016564:Amyloid beta-Protein Precursor / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000502:physiology; D016923:Cell Death; D002470:Cell Survival; D051360:Cyclin-Dependent Kinase 5 / Q000378:metabolism*; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D009474:Neurons / Q000502:physiology; D010300:Parkinson Disease / Q000503:physiopathology
D016564:Amyloid beta-Protein Precursor; D051360:Cyclin-Dependent Kinase 5; C495905:CDK5 protein, human