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Renieramycin T (RT) enhances apoptosis induction through Mcl-1 proteasomal degradation. Normally, Mcl-1 forms complex with Bak to inhibit its apoptotic function, but when Mcl-1 is degraded through the ubiquitin-mediated proteasomal degradation by treatment of RT, Bak is relieved. Activated Bak forms oligomerization that can permeabilize the outer membrane of mitochondria and release cytochrome c to initiate the apoptosis mechanism.
