Signaling induced by hop/STI-1 depends on endocytosis.

Autor: Americo TA; Instituto de Biofísica da UFRJ, Centro de Ciências da Saúde, bloco G, Cidade Universitária, Rio de Janeiro, Brazil., Chiarini LB, Linden R
Jazyk: angličtina
Zdroj: Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2007 Jun 29; Vol. 358 (2), pp. 620-5. Date of Electronic Publication: 2007 May 08.
DOI: 10.1016/j.bbrc.2007.04.202
Abstrakt: The co-chaperone hop/STI-1 is a ligand of the cell surface prion protein (PrP(C)), and their interaction leads to signaling and biological effects. Among these, hop/STI-1 induces proliferation of A172 glioblastoma cells, dependent on both PrP(C) and activation of the Erk pathway. We tested whether clathrin-mediated endocytosis affects signaling induced by hop/STI-1. Both hyperosmolarity induced by sucrose and monodansyl-cadaverine blocked Erk activity induced by hop/STI-1, without affecting the high basal Akt activity typical of A172. The endocytosis inhibitors also affected the sub-cellular distribution of phosphorylated Erk, consistent with blockade of the latter's activity. The data indicate that signaling induced by hop/STI-1 depends on endocytosis. These findings are consistent with a role of sub-cellular trafficking in signal transduction following engagement by PrP(C) by ligands such as hop/STI-1, and may help help unravel both the functions of the prion protein, as well as possible loss-of-function components of prion diseases.
Databáze: MEDLINE
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