| Caldesmon as a therapeutic target for proliferative vascular diseases. | |
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MedLine Citation:
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PMID: 18855735 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Chi-Ming Hai |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Review |
Journal Detail:
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Title: Mini reviews in medicinal chemistry Volume: 8 ISSN: 1389-5575 ISO Abbreviation: Mini Rev Med Chem Publication Date: 2008 Oct |
Date Detail:
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Created Date: 2008-10-15 Completed Date: 2009-01-07 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101094212 Medline TA: Mini Rev Med Chem Country: Netherlands |
Other Details:
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Languages: eng Pagination: 1209-13 Citation Subset: IM |
Affiliation:
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Department of Molecular Pharmacology, Physiology & Biotechnology, Brown University, Providence, Rhode Island 02912, USA. Chi-Ming_Hai@brown.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Actins
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metabolism Angioplasty Animals Calmodulin-Binding Proteins / pharmacology* Cell Movement Cell Proliferation Coronary Restenosis Gene Transfer Techniques Humans Metalloproteases / metabolism Models, Biological Phosphorylation Vascular Diseases / drug therapy* |
| Grant Support | |
ID/Acronym/Agency:
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HL-52714/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Actins; 0/Calmodulin-Binding Proteins; EC 3.4.-/Metalloproteases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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