作者: Shigeomi Shimizu , Yosuke Matsuoka , Yasuo Shinohara , Yoshihiro Yoneda , Yoshihide Tsujimoto
关键词: Transfection 、 Cytochrome c 、 Mitochondrial apoptosis-induced channel 、 Bcl-2 Homologous Antagonist-Killer Protein 、 Molecular biology 、 Voltage-dependent anion channel 、 Apoptosis 、 Mitochondrion 、 Biology 、 Bcl-2-associated X protein 、 Cell biology
摘要: Through direct interaction with the voltage-dependent anion channel (VDAC), proapoptotic members of Bcl-2 family such as Bax and Bak induce apoptogenic cytochrome c release in isolated mitochondria, whereas BH3-only proteins Bid Bik do not directly target VDAC to release. To investigate biological significance for apoptosis mammalian cells, we produced two kinds anti-VDAC antibodies that inhibited activity. In these prevented Bax-induced loss mitochondrial membrane potential (Δψ), but Bid-induced When microinjected into antibodies, control also apoptosis, did prevent indicating is essential Bax-induced, Bid-induced, changes apoptotic cell death. addition, microinjection significantly etoposide-, paclitaxel-, staurosporine-induced apoptosis. Furthermore, used show Bax- Bak-induced lysis red blood cells was mediated by on plasma membrane. Taken together, our data provide evidence plays an role cells.