Estudo Funcional de Mutantes da Proteína Prion Celular Associados à Doenças por Prion

with neurites was quantified in each condition. ERK1/2 phosphorylation in Prnp+/+ (n=4; C) or in Prnp0/0 (n=3) neurons (D) treated with Ln `)`1 peptide (37 f,LM) at different time points (0.5 to 30 min) determined by immunoblotting with antibodies against ERK1/2 (ERK) or against the phosphorylated form of the enzyme (pERK). Relative levels of enzyme activity represent the ratio between phosphorylated ERK1/2 and total ERK, normalized to the untreated group (ctr). E) PKC activity in Prnp+/+ (solid bars) or Prnp0/0 neurons (open bars) treated or not (ctr) with Ln `)`1 peptide (37 f,LM) at different time points (0.5 to 30 min; n=4). PMA was used as an internal control for PKC activation, and BIM is a specific PKC inhibitor (n=4). F) PKA activity in Prnp+/+ (solid bars) or Prnp0/0 neurons (open bars) treated with Ln `)`1 peptide at different time points (0.5 to 30 min; n=3). Forskolin (10 f,LM Forsk) was used as an internal control of PKA activation (n=3). Results represent means ± se of independent experiments analyzed and compared by 2-way ANOVA and Newman-Keuls post hoc test (A) or 1-way ANOVA and Newman-Keuls post hoc test (B, E, F). *Statistical significance when compared to control cells without treatment, *P < 0.01 (A), *P < 0.05 (B, C, E, F) vs. control.…