Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Sato, Y. et al.

Overexpression of N-acetylglucosaminyltransferase III enhances the epidermal growth factor- induced phosphorylation of ERK in HeLaS3 cells by up-regulation of the internalization rate of the receptors.

N-Acetylglucosaminyltransferase III (GnT-III) is a key enzyme that inhibits the extension of N-glycans by introducing a bisecting N-acetylglucosamine residue. In this study we investigated the effect of GnT-III on epidermal growth factor (EGF) signaling in HeLaS3 cells. Although the binding of EGF to the epidermal growth factor receptor (EGFR) was decreased in GnT-III transfectants to a level of about 60% of control cells, the EGF- induced activation of extracellular signal-regulated kinase ( ERK) in GnT-III transfectants was enhanced to approximately 1.4-fold that of the control cells. A binding analysis revealed that only low affinity binding of EGF was decreased in the GnT-III transfectants, whereas high affinity binding, which is considered to be responsible for the downstream signaling, was not altered. EGF- induced autophosphorylation and dimerization of the EGFR in the GnT-III transfectants were the same levels as found in the controls. The internalization rate of EGFR was, however, enhanced in the GnT-III transfectants as judged by the uptake of (125)I-EGF and Oregon Green-labeled EGF. When the EGFR internalization was delayed by dansylcadaverine, the up-regulation of ERK phosphorylation in GnT-III transfectants was completely suppressed to the same level as control cells. These results suggest that GnT-III overexpression in HeLaS3 cells resulted in an enhancement of EGF- induced ERK phosphorylation at least in part by the up-regulation of the endocytosis of EGFR.[1]

References

Overexpression of N-acetylglucosaminyltransferase III enhances the epidermal growth factor-induced phosphorylation of ERK in HeLaS3 cells by up-regulation of the internalization rate of the receptors. Sato, Y., Takahashi, M., Shibukawa, Y., Jain, S.K., Hamaoka, R., Miyagawa Ji, n.u.l.l., Yaginuma, Y., Honke, K., Ishikawa, M., Taniguchi, N. J. Biol. Chem. (2001) [Pubmed]

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