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Bcl-xL is a key anti-apoptotic protein that regulates programmed cell death (apoptosis). It inhibits mitochondrial outer membrane permeabilization, preventing the release of pro-apoptotic factors and subsequent caspase activation. Overexpression of BCL-xL contributes to cancer cell survival and resistance to chemotherapy, making it a therapeutic target. Strategies include PROTACs and small molecules disrupting its interactions.
Inhibition of pro-apoptotic protein interactions, prevention of mitochondrial outer membrane permeabilization and cytochrome c release, inhibition of caspase activation
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