CDK5 Human

Cdk5 was first discovered due to its sequence homology to the human cell division cycle protein 2 (Cdc2, also known as Cdk1), a key regulator of cell cycle progression . Despite its similarity to other Cdks, Cdk5’s activity is most prominent in post-mitotic neurons, particularly in the adult brain . The kinase activity of Cdk5 is regulated by its association with a non-cyclin protein called p35, which activates Cdk5 upon binding .

Cdk5 is highly expressed in the nervous system, where it phosphorylates a multitude of substrates involved in neuronal proliferation, differentiation, migration, and synaptic plasticity . During brain development, the expression and kinase activity of Cdk5 increase significantly, correlating with the main phase of neuronal differentiation . This kinase is essential for proper brain development and the maintenance of neuronal functions.

There is increasing evidence that aberrant Cdk5 activity is associated with various neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and Amyotrophic lateral sclerosis (ALS) . Dysregulation of Cdk5 can lead to neuronal damage and death, contributing to the pathogenesis of these diseases. Research has shown that Cdk5 is involved in processes such as mitochondrial dysfunction, oxidative stress, and neuroinflammation, which are common features of neurodegeneration .

Human recombinant Cdk5 is produced using recombinant DNA technology, typically expressed in bacterial systems like E. coli . This recombinant form is used in various research applications to study the kinase’s function, regulation, and involvement in diseases. The availability of human recombinant Cdk5 allows for detailed biochemical and physiological studies, providing insights into its role in health and disease .