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. Author manuscript; available in PMC: 2010 Aug 1.
Published in final edited form as: Biochem Pharmacol. 2009 Apr 14;78(3):241–248. doi: 10.1016/j.bcp.2009.04.005

Fig. 5. Model depicting the main findings.

Fig. 5

In control KB-3 cells, Bcl-xL interacts with Bax in the cytosol, and vinblastine induces JNK-dependent Bax mitochondrial translocation. JNK may also directly phosphorylate Bax, and a kinase distinct from JNK phosphorylates Bcl-xL (15). At the mitochondria, Bax induces cell death which is antagonized by Bcl-xL overexpression. GFP-Bax when transiently expressed in KB-3 localizes to the mitochondria and induces cell death, and this too is antagonized by Bcl-xL overexpression.