Skip to main content
. Author manuscript; available in PMC: 2014 Jan 28.
Published in final edited form as: J Biol Chem. 2004 Oct 19;279(52):54140–54152. doi: 10.1074/jbc.M410493200

Fig. 4. 14-3-3τ is required for the stabilization of E2F1 protein upon DNA damage.

Fig. 4

A, knockdown of 14-3-3τ blocks the induction of endogenous E2F1 by adriamycin treatment. HEK293 cells were transfected with 14-3-3τ siRNA and treated with adriamycin (5 μM) for 0–24 h. Western blot analysis (IB) was performed using antibodies as indicated. B, 14-3-3τ siRNA inhibits adriamycin-induced prolongation of E2F1 half-life. HEK293 cells were transfected with an empty vector (upper panels) or 14-3-3τ siRNA (lower panels) and were either left untreated (left panels) or treated with adriamycin (5 μM) for 24 h (right panels). The cells were then treated with cycloheximide (CHX; 20 μg/ml) for the time periods as indicated. The endogenous E2F1 protein was detected by Western blot analysis. C, The E2F1 levels in B were quantified by densitometry, and the relative abundance of E2F1 following CHX treatment was compared with that seen without CHX treatment and plotted.