β-Actin: A Regulator of NOS-3

Sci. STKE, 18 September 2007
Vol. 2007, Issue 404, p. pe52
DOI: 10.1126/stke.4042007pe52

β-Actin: A Regulator of NOS-3

  1. Yunchao Su1,*,
  2. Dmitry Kondrikov1, and
  3. Edward R. Block1,2
  1. 1Department of Medicine, University of Florida College of Medicine, Gainesville, FL 32610, USA.
  2. 2Research Service, Malcom Randall Veterans Affairs Medical Center, Gainesville, FL 32608–1197, USA.
  1. *Corresponding author. E-mail, ysu{at}ufl.edu

Abstract

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.

Citation:

Y. Su, D. Kondrikov, and E. R. Block, β-Actin: A Regulator of NOS-3. Sci. STKE 2007, pe52 (2007).

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