The Journal of Neuroscience, December 7, 2005, ():
Interaction of Cellular Prion and Stress-Inducible Protein 1 Promotes Neuritogenesis and Neuroprotection by Distinct Signaling Pathways
J. Neurosci. Lopes et al.
25: 11330
Supplemental data
Files in this Data Supplement:
- supplemental material
-
Figure 9: Signaling pathway inhibitors had no effect upon staurosporine-induced cell death. Prnp+/+ hippocampal neurons were plated on poly-L-lysine and pre-treated with the inhibitors (Inhi), 5x10-5M U0; 5x10-7M Bim; 10-7M Chel or 6x10-8M Kt for 1h. Cell death was induced by treatment with 2.5x10-8M staurosporine (Stauro) for an additional 16h. The cells were fixed, stained with propidium iodide, and the percentage of pyknotic profiles, indicating cell death, was estimated. Values represent the mean and standard deviation (vertical bars) of at least three independent experiments. * p< 0.05 (Anova and Tukey post hoc test) vs. control.
- supplemental material
-
Figure 10: Interaction of STI1 with PrPc induces both neuritogenesis and neuroprotection through distinct signaling pathways. The cAMP-PKA dependent pathway is implicated in neuroprotection, demonstrated in both retinal (Chiarini et al., 2002; Zanata et al., 2002) and hippocampal neurons, whereas MAPK signaling is involved in neuritogenesis. There are at least three possibilities for the PrPc-STI1 complex formation: proteins can interact in the same (A) or in distinct cells (B) or STI1 can act as a secreted neurotrophic factor (C)
