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.
Department of Physiology, University of Oklahoma Health Sciences Center, College of Medicine, Oklahoma City, OK 73104, USA. qing-guo@ouhsc.edu
Qing
Q
Guo
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