Tg-ESAs significantly down-regulated the levels of βIII-tubulin and GFAP in C17.2 cells in a dose-dependent manner.
Tg-ESAs significantly decreased β-catenin level in nucleus of C17.2 cells treated with wnt3a, an activator of Wnt pathway.
A new mechanism for T. gondii infection-induced neuropathogenesis: blockade of Wnt/β-catenin pathway in NSCs by Tg-ESAs.