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beta-Actin: A Regulator of NOS-3

β-actin is traditionally considered a structural protein that organizes and maintains the shape of nonmuscle cells, although data now indicate that β-actin is also a signaling molecule. β-actin is directly associated with nitric oxide synthase type 3 (NOS-3) in endothelial cells and platelets, and this interaction increases NOS-3 activity and the affinity of NOS-3 for heat shock protein 90 kD (Hsp90). The β-actin–induced increase in NOS-3 activity may be caused directly by β-actin, the binding of Hsp90 to NOS-3, or both. Alterations in the interaction between β-actin and NOS-3 could be caused by changes either in the availability of β-actin or in the affinity of NOS-3 for β-actin, and these alterations probably contribute to vascular complications and platelet aggregation. Studies examining the interactions between NOS-3, β-actin, and Hsp90 could potentially lead to the discovery of effective peptides for the treatment of diseases associated with impaired NOS-3 activity and nitric oxide release, such as systemic and pulmonary hypertension, atherosclerosis, and thrombotic diseases.

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Resource Type: Bibliography, Diagram, Illustration, Journal article/Issue, Review
Audience Level: Undergraduate upper division 15-16, Graduate, Professional (degree program)

Author and Copyright

Authors and Editors: Yunchao Su of Department of Medicine, University of Florida College of Medicine, Dmitry Kondrikov of Department of Medicine, University of Florida College of Medicine, Edward R. Block of Department of Medicine, University of Florida College of Medicine
Publisher: American Association for the Advancement of Science
Format: application/pdf, image/gif, image/jpeg, text/html
Copyright and other restrictions: Yes
Cost: Yes


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