Presenting a considerable disease burden and global health threat, hepatocellular carcinoma (HCC) is in desperate need of potent and effective therapies. p53-Bad* is designed to provide mitochondrial targeting, enhance binding interactions with antiapoptotic Bcl-2 family members, and improve apoptotic activity in various cancers. While we have shown that fusion of p53 and Bad* improves mitochondrial localization and increases apoptosis in HCC, critically, the mechanism of action and nature of this heightened apoptotic function have not been delineated.
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