| Violaceols Function as Actin Inhibitors Inducing Cell Shape Elongation in Fibroblast Cells. | |
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MedLine Citation:
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PMID: 22878183 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Violaceol-I and -II were isolated from a fractionated library of marine-derived fungal metabolites. These compounds increased the calcium ion concentration inside the cell and caused F-actin aggregation in rat fibroblast 3Y1 cells within 3 h resulting in cell shape elongation. Calcium chelator BAPTA-AM (1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetrakis (acetoxymethyl ester) inhibited violaceol-I- and -II-induced F-actin aggregation in 3Y1 cells, and hence violaceol-I- and -II act in a calcium dependent manner. Violaceol-I and -II inhibited G-actin polymerization in vitro in a dose-dependent manner and strongly associated with G-actin, at dissociation equilibrium constants of 1.44 × 10<sup>-8</sup> M and 2.52 × 10<sup>-9</sup> M respectively. Here we report the identification of a novel function of violaceol-I and -II as actin inhibitors. Violaceol-I and -II induced cell shape elongation through F-actin aggregation in 3Y1 fibroblasts. These compounds may give researchers new insights into the role of actin in tumorigenesis and lead to the development of additional anti-tumor drugs. |
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Authors:
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Yukihiro Asami; Jae-Hyuk Jang; Hyuncheol Oh; Jae Hak Sohn; Jong Won Kim; Dong Oh Moon; Osong Kwon; Makoto Kawatani; Hiroyuki Osada; Bo Yeon Kim; Jong Seog Ahn |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-8-07 |
Journal Detail:
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Title: Bioscience, biotechnology, and biochemistry Volume: - ISSN: 1347-6947 ISO Abbreviation: Biosci. Biotechnol. Biochem. Publication Date: 2012 Aug |
Date Detail:
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Created Date: 2012-8-10 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9205717 Medline TA: Biosci Biotechnol Biochem Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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Chemical Biology Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB). |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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