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Identification of Inhibitors Against BAK Pore Formation using an Improved in vitro Assay System
송승수,이원규,Sreevidya Aluvila,오경준,유연규 대한화학회 2014 Bulletin of the Korean Chemical Society Vol.35 No.2
The pro-apoptotic BCL-2 family protein BID activates BAK and/or BAX, which form oligomeric pores in the mitochondrial outer membrane. This results in the release of cytochrome c into the cytoplasm, initiating the apoptotic cascade. Here, we utilized liposomes encapsulating sulfo-rhodamine at a controlled temperature to improve upon a previously reported assay system with enhanced sensitivity and specificity for measuring membrane permeabilization by BID-dependent BAK activation. BAK activation was inhibited by BCL-XL protein but not by a mutant protein with impaired anti-apoptotic activity. With the assay system, we screened a chemical library and identified several compounds including trifluoperazine, a mitochondrial apoptosisinduced channel blocker. It inhibited BAK activation by direct binding to BAK and blocking the oligomerization of BAK.
Identification of Inhibitors Against BAK Pore Formation using an Improved in vitro Assay System
Song, Seong-Soo,Lee, Won-Kyu,Aluvila, Sreevidya,Oh, Kyoung Joon,Yu, Yeon Gyu Korean Chemical Society 2014 Bulletin of the Korean Chemical Society Vol.35 No.2
The pro-apoptotic BCL-2 family protein BID activates BAK and/or BAX, which form oligomeric pores in the mitochondrial outer membrane. This results in the release of cytochrome c into the cytoplasm, initiating the apoptotic cascade. Here, we utilized liposomes encapsulating sulfo-rhodamine at a controlled temperature to improve upon a previously reported assay system with enhanced sensitivity and specificity for measuring membrane permeabilization by BID-dependent BAK activation. BAK activation was inhibited by BCL-$X_L$ protein but not by a mutant protein with impaired anti-apoptotic activity. With the assay system, we screened a chemical library and identified several compounds including trifluoperazine, a mitochondrial apoptosis-induced channel blocker. It inhibited BAK activation by direct binding to BAK and blocking the oligomerization of BAK.