Abstract
Caldesmon is a negative regulator of cell proliferation, migration, and metalloproteinase release. Caldesmon function is regulated by multiple kinases, targeting multiple phosphorylation sites. Recently, overexpression of caldesmon has been shown to inhibit neointimal formation after experimental angioplasty, suggesting that caldesmon may be a potential therapeutic target for proliferative vascular diseases.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Actins / metabolism
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Angioplasty
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Animals
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Calmodulin-Binding Proteins / pharmacology*
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Cell Movement
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Cell Proliferation
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Coronary Restenosis
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Gene Transfer Techniques
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Humans
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Metalloproteases / metabolism
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Models, Biological
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Phosphorylation
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Vascular Diseases / drug therapy*
Substances
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Actins
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Calmodulin-Binding Proteins
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Metalloproteases