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.
|Autori:||Mattii L; Battolla B; Azzarà A; D'Urso G; Montali U; Petrini M.|
|Titolo:||Glycosylation interference on RhoA activation: focus on G-CSF|
|Anno del prodotto:||2011|
|Digital Object Identifier (DOI):||10.1016/j.leukres.2010.05.027|
|Appare nelle tipologie:||1.1 Articolo in rivista|