The apoptotic response in HCT116BAX-/-cancer cells becomes rapidly saturated with increasing expression of a GFP-BAX fusion protein |
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| Authors: | Sheila J Semaan Robert W Nickells |
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| Affiliation: | 1.Department of Ophthalmology and Visual Sciences, Medical Sciences Center,University of Wisconsin, School of Medicine and Public Health,Madison,USA;2.Department of Biomolecular Chemistry, Medical Sciences Center,University of Wisconsin, School of Medicine and Public Health,Madison,USA;3.Department of Reproductive Medicine,University of California, San Diego,La Jolla,USA |
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| Abstract: | Background Many chemotherapeutic agents promote tumor cell death by activating the intrinsic pathway of apoptosis. Intrinsic apoptosis involves permeabilization of the mitochondrial outer membrane and the release of cytochrome c, a process that is controlled by proteins of the BCL2 gene family. Chemoresistance is often associated with abnormalities in concentrations of BCL2 family proteins. Although stoichiometirc interactions between anti-apoptotic and BH3-only BCL2 family proteins have been well documented as affecting cell death, the association between changes in BAX concentration and intrinsic apoptosis are poorly understood. |
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