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- W171161698 abstract "Posttranslational modifications of small GTPases regulate enzyme activity and subcellular localization, resulting in altered cellular functions. The role of small-GTPase carboxyl methylation in modulating endothelial functions is not well understood. In our study, we have used cultured endothelial cells to assess the effects of inhibition of carboxyl methylation on endothelial cell function. We have found that isoprenylcysteine carboxyl methyltransferase (ICMT) inhibitors cause relocalization of focal adhesion complexes and apoptosis of endothelial cells. This is accompanied by decreased carboxyl methylation and decreased activation of Ras GTPase. Furthermore, overexpression of Ras prevents apoptosis caused by the ICMT inhibitor adenosine/homocysteine. Thus, we conclude that inhibition of Ras carboxyl methylation causes endothelial cell apoptosis. We have also found that ICMT inhibitors decrease endothelial cell migration and monolayer permeability, an effect that may be related to impaired RhoA carboxyl methylation and activation. Thus, it is evident that altered small-GTPase methylation has multiple effects on endothelial cell functions." @default.
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- W171161698 date "2005-01-01" @default.
- W171161698 modified "2023-10-16" @default.
- W171161698 title "Carboxyl Methylation of Small GTPases and Endothelial Cell Function" @default.
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- W171161698 doi "https://doi.org/10.1007/978-1-59259-909-7_7" @default.
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