Glycosylation interference on RhoA activation: Focus on G-CSF |
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Authors: | Letizia Mattii Barbara BattollaAntonio Azzarà Giuseppina D’UrsoUmberto Montali Mario Petrini |
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Institution: | a Department of Human Morphology and Applied Biology, Medical Histology and Embryology Section, University of Pisa, Via Roma 55, 56126 Pisa, Italy b Department of Oncology Transplant and Advanced Technologies in Medicine, Hematology Division, University of Pisa, Pisa, Italy c Department of Human and Environmental Sciences, Medical Chemistry and Biochemistry Section, University of Pisa, Pisa, Italy |
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Abstract: | Glycosylation of cytokines appears to be responsible for several differences in their activity, and focusing on G-CSF, several divergences between the non-glycosylated G-CSF, Filgrastim, and the glycosylated G-CSF, Lenograstim, have been reported. To verify the role of G-CSF glycosylation in mediating these differences we tested in vitro the effects on the RhoA activation of the different G-CSFs, including deglycosylated Lenograstim. The results showed that Filgrastim induced sustained-RhoA activation while Lenograstim did not do so. Deglycosylated Lenograstim mimicked Filgrastim, resulting in RhoA hyper-activation. These in vitro findings demonstrate that the glycosylation of G-CSF plays a crucial role in RhoA activation. |
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Keywords: | G-CSF Glycosylation RhoA |
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