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. Author manuscript; available in PMC: 2009 Jun 8.
Published in final edited form as: Eur J Neurosci. 2009 Mar;29(6):1119–1130. doi: 10.1111/j.1460-9568.2009.06664.x

FIG. 2.

FIG. 2

Effects of murine recombinant 3K3A-APC on activation of caspases-9 and -3, p53 levels and Bax and Bcl-2 expression in NMDA-treated mouse neurons. Caspase-9 (a) and caspase-3 (b) activities in neurons treated with NMDA in the absence or presence of caspase-9 inhibitor (10 µm; z-LEDH-fmk) and/or caspase-3 inhibitor (50 µm; Ac-DEVD-CHO), murine 3K3A-APC, wt-APC and enzymatically inactive S360A-APC at 5 nm. (c) Western blots for p53 in nuclear extracts, Bax and Bcl-2 in whole-cell extracts from NMDA-treated cells in the absence or presence of murine 3K3A-APC (5 nm). Histone H1 was used as a control for loading of nuclear proteins and β-actin as a control for loading of the whole-cell lysate proteins. (d) Intensity of p53, Bax and Bcl-2 signals measured by scanning densitometry and effects of 3K3A-APC in experiments as in (c). Signal for nuclear p53 was normalized by histone H1 abundance, and signal for Bax and Bcl-2 with β-actin. All values are mean + SEM. NS, non-significant.