alexa Nucleocytoplasmic Cdk5 is involved in neuronal cell cycle and death in post-mitotic neurons.
Neurology

Neurology

Brain Disorders & Therapy

Author(s): Zhang J, Herrup K

Abstract Share this page

Abstract In a variety of neurodegenerative disease, despite the frequent correlation of neuronal cell cycle and cell death in the same neuronal populations, the mechanistic pathway linking the two remains undefined. One possible link is the atypical cyclin dependent kinase, Cdk5. Cdk5 exerts a double protective function in neurons, first by suppressing the cell cycle in the nucleus and second by suppressing cell death in the cytoplasm. Cdk5 transport between nucleus and cytoplasm serves to regulate the balance between these two events. Cdk5 nuclear localization relies on its interaction with p27, and its cell cycle suppression activity is achieved by direct binding to E2F1, disrupting the DP1-E2F1 dimer and its DNA binding ability. To bind to E2F1, Cdk5 does not need to be catalytically active but it does require a physical association with both p27 and its cyclin-like activator, p35. Because of this requirement, the proper levels and locations of p27 and p35 are characteristics that endow a neuron a unique form of cell cycle regulation that uses Cdk5 in a non-catalytic role. The findings offer cautionary notes to any strategy aimed at blocking Cdk5 activity as a means of combating neurodegenerative disease. To the extent that these approaches either directly or indirectly influence Cdk5 levels or location, they may produce unexpected and possibly unwanted consequences. This article was published in Cell Cycle and referenced in Brain Disorders & Therapy

Recommended Conferences

Relevant Topics

Peer Reviewed Journals
 
Make the best use of Scientific Research and information from our 700 + peer reviewed, Open Access Journals
International Conferences 2017-18
 
Meet Inspiring Speakers and Experts at our 3000+ Global Annual Meetings

Contact Us

Agri, Food, Aqua and Veterinary Science Journals

Dr. Krish

[email protected]

1-702-714-7001 Extn: 9040

Clinical and Biochemistry Journals

Datta A

[email protected]

1-702-714-7001Extn: 9037

Business & Management Journals

Ronald

[email protected]

1-702-714-7001Extn: 9042

Chemical Engineering and Chemistry Journals

Gabriel Shaw

[email protected]

1-702-714-7001 Extn: 9040

Earth & Environmental Sciences

Katie Wilson

[email protected]

1-702-714-7001Extn: 9042

Engineering Journals

James Franklin

[email protected]

1-702-714-7001Extn: 9042

General Science and Health care Journals

Andrea Jason

[email protected]

1-702-714-7001Extn: 9043

Genetics and Molecular Biology Journals

Anna Melissa

[email protected]

1-702-714-7001 Extn: 9006

Immunology & Microbiology Journals

David Gorantl

[email protected]

1-702-714-7001Extn: 9014

Informatics Journals

Stephanie Skinner

[email protected]

1-702-714-7001Extn: 9039

Material Sciences Journals

Rachle Green

[email protected]

1-702-714-7001Extn: 9039

Mathematics and Physics Journals

Jim Willison

[email protected]

1-702-714-7001 Extn: 9042

Medical Journals

Nimmi Anna

[email protected]

1-702-714-7001 Extn: 9038

Neuroscience & Psychology Journals

Nathan T

[email protected]

1-702-714-7001Extn: 9041

Pharmaceutical Sciences Journals

John Behannon

[email protected]

1-702-714-7001Extn: 9007

Social & Political Science Journals

Steve Harry

[email protected]

1-702-714-7001 Extn: 9042

 
© 2008-2017 OMICS International - Open Access Publisher. Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version
adwords