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. 2011 Jan 14;18(6):1024–1035. doi: 10.1038/cdd.2010.175

Figure 9.

Figure 9

Bcl-2 deleted of its BH4 domain is not a dominant-negative inhibitor of the endogenous wild-type (wt) bcl-2 protein. (a) Western blot analysis of bcl-2 protein expression, and (b)VEGF protein expression evaluated by ELISA in HT29 colon carcinoma cell line and its derivative clones overexpressing wt bcl-2 (Bcl-2/1, Bcl-2/2), or bcl-2 deleted of the BH4 domain (BH4 del/1, BH4 del/2). (c) VEGF protein expression evaluated by ELISA, and (d) western blot analysis of HIF-1α and VEGF proteins in HT29 cells after exposure to hypoxia in presence of 2 μM TAT–BH4 or TAT–CTRL as control. (a and d) Western blot representative of three independent experiments with similar results are shown. β-actin is shown as loading and transferring control. (b and c) Results represent the average±S.D. of three independent experiments. (b) P-values were calculated from control and wt or mutated bcl-2-overexpressing cells exposed at the same experimental conditions (*P<0.01). (c) P-values were calculated between control and TAT–BH4-treated cells exposed to hypoxia (*P<0.01)