Caldesmon as a therapeutic target for proliferative vascular diseases.
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.
Department of Molecular Pharmacology, Physiology & Biotechnology, Brown University, Providence, Rhode Island 02912, USA. Chi-Ming_Hai@brown.edu
Chi-Ming
CM
Hai
D000199:Actins / Q000378:metabolism; D017130:Angioplasty; D000818:Animals; D002148:Calmodulin-Binding Proteins / Q000494:pharmacology*; D002465:Cell Movement; D049109:Cell Proliferation; D023903:Coronary Restenosis; D018014:Gene Transfer Techniques; D006801:Humans; D045726:Metalloproteases / Q000378:metabolism; D008954:Models, Biological; D010766:Phosphorylation; D014652:Vascular Diseases / Q000188:drug therapy*
D000199:Actins; D002148:Calmodulin-Binding Proteins; D045726:Metalloproteases