RhoA mediates oligomeric Aβ42-induced neurotoxicity. A. N2A cells were transiently transfected with RhoA wild type, dominant-negative T19N mutant, or vector control; treated with oAβ42 for 24 hours; and assayed for neurotoxicity as described in Figure Legend 1. Significant difference (p < 0.01) between cells ± RhoA dominant-negative T19N mutant are indicated by an asterisk (*). Inset, expression levels of HA-taged RhoA were characterized by anti-HA antibody (Roche) with Western blot analysis with an equal amount of lysate from cells transfected vector, RhoA wild type or RhoA dominant-negative T19N mutant. B. N2A cells were transiently trasfected with RhoA wild type or dominant-negative T19N mutant expression plasmids. 48 hours post-transfection, cells were treated with 10 μM oAβ42 for 30 minutes, fixed and stained for Aβ with Aβ42 specific antibody (Invitrogen, green). RhoA wild type or T19N mutant transfected cells were identified by anti-HA antibody (red). Nuclei appear blue as detected by DAPI staining. Cells were individually outlined and mean fluorescence intensity of Aβ signals were quantified with NIH image software. Significant difference (p < 0.01) between cells transfected with RhoA wild type and T19N mutant is indicated by an asterisk (*).