Beta-actin: a regulator of NOS-3

Sci STKE. 2007 Sep 18;2007(404):pe52. doi: 10.1126/stke.4042007pe52.


Beta-actin is traditionally considered a structural protein that organizes and maintains the shape of nonmuscle cells, although data now indicate that beta-actin is also a signaling molecule. beta-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 beta-actin-induced increase in NOS-3 activity may be caused directly by beta-actin, the binding of Hsp90 to NOS-3, or both. Alterations in the interaction between beta-actin and NOS-3 could be caused by changes either in the availability of beta-actin or in the affinity of NOS-3 for beta-actin, and these alterations probably contribute to vascular complications and platelet aggregation. Studies examining the interactions between NOS-3, beta-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.

Publication types

  • Review

MeSH terms

  • Actins / chemistry
  • Actins / physiology*
  • Animals
  • Blood Platelets / metabolism
  • Cell Compartmentation
  • Cells, Cultured / metabolism
  • Endothelial Cells / metabolism
  • Enzyme Induction
  • HSP90 Heat-Shock Proteins / chemistry
  • HSP90 Heat-Shock Proteins / physiology*
  • Humans
  • Mice
  • Models, Biological
  • Nitric Oxide Synthase Type III / chemistry
  • Nitric Oxide Synthase Type III / genetics
  • Nitric Oxide Synthase Type III / physiology*
  • Protein Binding
  • Protein Conformation
  • Protein Interaction Mapping
  • Serum Response Element
  • Serum Response Factor / physiology
  • Sus scrofa


  • Actins
  • HSP90 Heat-Shock Proteins
  • Serum Response Factor
  • NOS3 protein, human
  • Nitric Oxide Synthase Type III